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		<title>Gastric Dilatation Volvulus (Bloat) update</title>
		<link>http://webcanine.com/2010/gastric-dilatation-volvulus-bloat-update/</link>
		<comments>http://webcanine.com/2010/gastric-dilatation-volvulus-bloat-update/#comments</comments>
		<pubDate>Mon, 06 Sep 2010 15:55:12 +0000</pubDate>
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				<category><![CDATA[Bloat (GDV)]]></category>
		<category><![CDATA[bloat risk]]></category>
		<category><![CDATA[prevention/treatment of bloat]]></category>

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		<description><![CDATA[<p>Gary W. Ellison, DVM, MS, DACVS
University of Florida
Gastric dilatation Volvulus complex also know as bloat is a medical and surgical emergency which is know to primarily affect large and giant breeds of dogs. The disease has also been reported in smaller breeds such as the Pekingese and Dachshund. Mortality has been estimated as high as 30 <span style="color:#777"> . . . &#8594; Read More: <a href="http://webcanine.com/2010/gastric-dilatation-volvulus-bloat-update/">Gastric Dilatation Volvulus (Bloat) update</a></span>]]></description>
			<content:encoded><![CDATA[<p>Gary W. Ellison, DVM, MS, DACVS<br />
University of Florida<br />
Gastric dilatation Volvulus complex also know as bloat is a medical and surgical emergency which is know to primarily affect large and giant breeds of dogs. The disease has also been reported in smaller breeds such as the Pekingese and Dachshund. Mortality has been estimated as high as 30 percent. There are no reliable estimates of how many dogs develop bloat in the United States each year, but in certain breeds such as Irish Setters and Great Danes owners reported an incidence of seven and ten percent respectively. It does appear that purebred dogs are more likely to develop bloat than are mixed breed dogs.<span id="more-1083"></span></p>
<p><strong>Results of Retrospective Studies<br />
Incidence </strong> Several recent reviews by Dr. Larry Glickman at Purdue University utilizing information from the veterinary medical database (VMDB) have discovered some interesting findings:<br />
1) Amongst veterinary institutions the frequency of bloat amongst all dogs ranged from 2.9-6.8 per 1000 dogs<br />
2) Approximately 29 percent of the dogs with gastric dilatation and 33 percent of those with dilatation and volvulus died.<br />
3) Aging of the dog increased risk. Dogs greater than seven years of age are more than twice as likely to have bloat as dogs 2-4 years of age.<br />
4) Purebreds were three times as likely to have bloat as mixed breed dogs.<br />
5) Males are twice as likely to bloat as females yet spaying or neutering has no effect on the risk of bloat.</p>
<p><strong>Studies of Risk Factors</strong><br />
Several risk factors have been identified which may contribute to the establishment of bloat in<br />
purebred dogs.</p>
<p><strong>Breed </strong> Bloat has been long reported to be more common in large and giant breeds of dogs yet until recently the prevalence of bloat was not compared to the dog population at large. When this data was analyzed statistically, it was found that the Great Dane, St. Bernard, Weimaraner, Irish Setter and Gordon Setter were breeds at greatest risk. An accompanying chart outlines the remainder of the breeds (Table 1).</p>
<p><strong>Chest Conformation </strong> Although it is established that large and giant breeds are the breeds at greatest risk it has been shown there are profound differences in the risk of bloat within certain<br />
breeds. This possibility seems related to conformation of the naimal’s chest. For instance, breeds such as Irish Setters which are at high risk may weigh approximately the same as some of the Retriever breeds yet the Retrievers are at much lower risk than Irish Setters for developing bloat. When looking at this more scientifically it was found that the depth and width of the chest may be the key in predicting which animals within a certain breed may develop bloat. It appears that the chest depth/width ration is highly correlated with risk of bloat, ie. Those animals with deep, narrow chests within a certain breed are much more likely to develop bloat than those dogs with deep wide chests. In using external measurements of chest conformation it was found that within the Great Dane breed the depth/width ration may indeed be useful in identifying animals prone to bloat. Also, Great Danes with moderate and high abdominal height to width rations were approximately 5 1⁄2 to 8 times as likely to develop bloat as those with low abdominal height to width rations. In Irish Setters the chest height to width ration also correlated with those dogs having a higher depth to width ration being much more likely to develop bloat than those animals<br />
with a lower depth to width ration. This information is obviously very significant in terms of<br />
selective breeding for the reduction of bloat in these breeds.</p>
<p><strong>Diet </strong> Exact determinations of types of diet on risk for developing bloat still cannot be made. Although cereal-based diets have incriminated, it is difficult to compare groups since almost all large and giant breeds are fed cereal-based diets. Therefore, further controlled studies will be necessary to determine if cereal-based diets are in fact a risk factor. However, several interesting findings have come to surface with regard to the diet and nutritional management of breeds predisposed to bloat. For instance, it has been shown that dogs who eat one meal a day are almost twice as likely to develop bloat as those fed twice a day. The rate of eating is also very important. Those dogs characterized as slow eaters have the lowest incidence of bloat whereas those dogs characterized as moderately fast eaters have about 2 1⁄2 times the chance of developing bloat and those characterized as fast eaters have almost five times the chance of developing bloat as those being characterized as slow eaters.<br />
Body weight may also be of some significance. Being overweight actually reduced the incidence<br />
of bloat compared to dogs that were optimum weight. However, those animals characterized as<br />
significantly underweight were about three times as likely to develop bloat as those animals<br />
characterized as optimum weight.</p>
<p><strong>Gender </strong> It has been shown that males are approximately twice as likely to develop bloat as females. Neutering does not seem to have an effect on the incidence however.</p>
<p><strong>Personality and Environment</strong> There does seem to be a direct correlation of the animal’s temperament relating to its tendency to develop bloat. Those animals being characterized as<br />
unhappy or fearful were about 2 1⁄2 times as likely to develop bloat as those animals characterized<br />
as happy. In addition, the environment may play a role. Stress appears to also significantly<br />
increase the chance of the animal developing bloat. Therefore, animals who may undergo<br />
significant stress traveling to show, etc. are tow to three times as likely to bloat than those<br />
animals who are not significantly affected by the transport. Also activity level may be important<br />
with those animals characterized as hyperactive and those animals being categorized as less<br />
active were twice as likely to develop bloat than those animals characterized as having a normal<br />
activity level.</p>
<p><strong>Summary and Conclusions</strong><br />
With regard to known epidemiologic factors affecting bloat some of the following recommendations can be made. It appears there is a correlation with chest and abdominal height/width ration with those animals having tall thin chests and abdomens more likely to develop bloat than those with lower, wider chests and abdomens, there selective breeding may<br />
possible be recommended to diminish the incidence due to conformation. With regard to diet and nutrition changes in feeding relating to twice a day feeding versus once a day feeding may be recommended. Also, changing the time of the meal is significant with those animals having constant changes in meal time being approximately 2 1⁄2 times as likely to develop bloat as those<br />
being fed at regular intervals. In addition, those animals undergoing a sudden increase in food<br />
intake are almost three times as likely to develop bloat as those animals kept on a regular food<br />
intake. Therefore, recommendations may be made to keep consistency and times of feeding regulated and to feed the moderate amount of food without sudden increases in the amount fed.<br />
It also appears that reducing the amount of stress on the animal will decrease the chances of<br />
bloating. Although no specific recommendations can be made about tranquilization knowing the<br />
temperament of your dog may help you in minimizing the amount of stress encountered during<br />
travel to and from shows. It also appears that keeping physical activity to a moderate amount<br />
that is what the animal is used to, will be more helpful in reducing the chances of bloat than allowing extra activity than normally expected.</p>
<p><strong>Etiology</strong><br />
The exact etiology of GDV is unknown, but it is most likely a multifactorial disease. Ingestion<br />
of cereal based diets and water followed by exercise is reported in some but not the majority of<br />
cases. Stretching of the hepatogastric or hepatoduodenal ligaments from chronic overeating may<br />
allow transposition of the stomach. Gastric outlet obstruction by foreign bodies has been observed in some cases but delayed gastric emptying caused by pyloric hypertrophy is not conclusively proven as a cause of GDV. Splenic torsion or displacement occurs secondarily to GDV rather than initiating it, as was once believed. Gas production secondary to bacterial fermentation by clostridial organisms is a postmortem finding and is not a source of gas in live animals. Aerophagia is a likely cause since gas composition of the gastric lumen resembles atmospheric air and the onset of GDV often follows vigorous exercise, excitement and barking.<br />
Recently there is evidence that gastric motility disorders may induce or follow GDV.</p>
<p><strong>Clinical Signs</strong><br />
Dogs usually demonstrate hypersalivation, retching or unproductive vomiting on presentation.<br />
Cranial abdominal distention is apparent and gastric tympany is usually present on blunt<br />
percussion of the right anterior quadrant. Hyperpnea or dyspnea accompanied by open mouth<br />
breathing indicates hypoxia due to reduced diaphragmatic excursions. Shock is evidenced by<br />
pale or injected mucous membranes, prolonged capillary perfusion, tachycardia and weak rapid<br />
femoral pulse.</p>
<p><strong>Mechanisms of Rotation</strong><br />
A lack of coordinated gastric contractions due to gastric myoelectric dysrhythmias may slow<br />
gastric emptying and contribute to the development of gastric dilatation volvulus (GDV). Food<br />
and fluid distension from overeating or gaseous distension from aerophagia causes intra-<br />
abdominal angulation of the gastroesophageal junction that prevents belching or vomiting.<br />
Gastric dilatation results. Volvulus occurs when the dilated gastric fundus becomes displaced<br />
from a left dorsal to a right ventral position. The pylorus concurrently shifts from its right<br />
ventral position to a left, caudal and dorsal position. When viewed from the rear a clockwise<br />
rotation occurs in the majority of the animals. The spleen follows the greater curvature to the<br />
right. The gastrosplenic ligament and short gastric arteries are often torn during the volvulus.</p>
<p><strong>Initial Management of GDV</strong><br />
Initial patient management involves shock therapy, and gastric decompression followed by<br />
management of cardiac arrhythmias. Shock therapy involves fluid loading with 90 ml/kg of<br />
lactated Ringers solution of the first hour. The use of hypertonic saline may also be beneficial,<br />
as it has been shown to be beneficial in increasing gastric arterial perfusion. Treatment for acid-<br />
base status is controversial with one study indicating normal pH and another indicating the<br />
presence of metabolic acidosis in cases of GDV. However, with mild metabolic acidosis Na<br />
bicarbonate infusion is not necessary as long as adequate volume replacement with lactated<br />
Ringers solution is achieved. Hypokalemia is a common finding associated with GDV and<br />
potassium replacement is sometimes warranted. Corticosteroids are administered after initial<br />
treatment with intravenous fluids. They cause vasodilation and improved tissue perfusion if fluid<br />
volume is adequate. Cardiac dysrhythmias are commonly seen and require careful pre- and<br />
postoperative management. Paroxysmal vent4ricular tachycardia, and premature ventricular<br />
contractions are most commonly seen.<br />
Gastric decompression is accomplished using a pre-measured, well lubricated PVC plastic foal<br />
nasogastric tube. Ability to pass the tube into the stomach does not mean that gastric volvulus is<br />
not present. If intubation is not possible in the prone position it is attempted in a sitting upright<br />
position. Sometimes trocharization is necessary to reduce distension and facilitate tube passage.<br />
The character of the fluid is sometimes important in predicting the status of the gastric lining.<br />
Black fetid smelling fluid with flecks of devitalized mucosa indicates that mucosal ischemia is<br />
present and often predicts the presence of gastric wall necrosis. After decompression, the<br />
stomach is lavaged with 4-5 liters of water using gravity flow, dose syringe or stomach pump.</p>
<p><strong>Radiography</strong><br />
Radiography is always postponed until after patient stabilization. With gastric dilatation the<br />
stomach appears as a grossly distended gas and fluid filled structure that occupies the cranial<br />
abdomen displacing all remaining viscera posteriorly. The spleen is usually not visible in its<br />
normal left ventral location and is often located in a right dorsal position. Gastric volvulus is<br />
suspected when the pylorus is located dorsal, cranial and to the left of the midline. After<br />
decompression it may take a classic “upside down” appearance. Left and right lateral views are<br />
recommended. On the right lateral view gas can be seen in the pylorus whereas on the left lateral<br />
view gas may be seen in the fundus. If stomach position is questionable barium sulfate is<br />
administered to identify the pylorus.</p>
<p><strong>Surgical Management</strong><br />
Definitive management of GDV involves 1) repositioning of the stomach with resection of any<br />
devitalized gastric wall and 2) a prophylactic gastropexy technique to prevent recurrence. UP to<br />
80 percent recurrence of GDV is reported with gastric decompression or repositioning alone.<br />
We now advocate laparotomy as soon as the patient is a reasonable anesthetic risk. This allows<br />
early derotation that increases circulation and allows assessment of gastric wall viability. Areas<br />
of necrosis are detected early and resected if possible. With 270o to360o clockwise gastric<br />
volvulus the dilated stomach is covered on its ventral aspect by omentum. Reduction is<br />
accompanied by passing the had down the left abdominal wall, grasping the pylorus in its left<br />
dorsal position and rotating it in a caudal and counter-clockwise manner to its normal right sided<br />
location.</p>
<p><strong>Gastrectomy Techniques</strong><br />
Standard methods for gastrectomy involve ligation of branches of the left gastroepileploic<br />
arteries and veins allowing areas along the greater curvature of the stomach to be resected. The<br />
stomach is resected back to areas of healthy bleeding. Spillage is likely and prevented through<br />
the use of Babcock forceps or stay sutures. After resection is complete the stomach is closed in<br />
two layers. The mucosa and submucosa are closed with a continuous inverted Cushing pattern of<br />
2-0 or 3-0 PDS or Maxon. The serosa and muscularis are then closed with a similar pattern.<br />
Recently we have relied heavily on the autostapling equipment for rapid gastrectomy procedures<br />
with minimum risk of spillage. The TA90 autostapler is used with the green (4.8 mm) or blue<br />
(3.5mm) cartridge. Often several end-to-end staple lines have to be placed since each staple line<br />
is only 9 cm in length. The surgeon needs to overlap the staple lines by a few mm to prevent<br />
leakage between the staples.</p>
<p><strong>Rationale for Gastropexy</strong><br />
By definition gastropexy describes the fixation of the stomach to nearby structures or body wall<br />
as a means of preventing recurrence of GDV. Although gastropexy procedures reportedly<br />
diminish the recurrency rate of DGV, their reliability in producing permanent adhesions between<br />
the stomach and abdominal wall is not well documented.<br />
Most North American surgeons use an antral gastropexy procedure to fix the gastric antrum to<br />
the right abdominal wall. The three major categories of “permanent” antral gastropexies used in<br />
North America are the tube gastrostomy described by Parks (1976); the incisional gastropexy<br />
described by MacCoy (1982); and the circumcostal gastropexy described by Fallah (1982). In<br />
addition, two modifications of muscle flap techniques, one using a “muscular flap” from the<br />
abdominal wall (Shulman, 1986) and another using a “belt-loop” from the gastric muscularis<br />
(Whitney, 1989), have recently been described.</p>
<p><strong>Clinical Results</strong><br />
Potential advantages of the tube gastropexy are that 1) the surgery is rapid and easy, 2) the tube<br />
not only creates a permanent adhesion of the gastric antrum to the abdominal wall preventing<br />
recurrence of volvulus but also 3) allows for continued gastric decompression in the early<br />
postoperative period and 4) slurried food or medications can be offered through the tube. The<br />
main disadvantages of the technique are 1) the nursing care and long hospital period required for<br />
tube management and 2) t6he potential for fatal peritonitis secondary to leakage around the tube<br />
or early removal by the dog.<br />
Clinical studies of the tube gastrostomy have yielded encouraging results. Flanders (1984)<br />
reported recurrence of volvulus in only one of 29 dogs treated with tube gastrostomy for a<br />
follow-up time ranging from 14 to 40 months. However there was a mortality rate of 31 percent<br />
during the first week after surgery. Johnson (1984) reported on 76 cases where this technique<br />
was used with only a five percent recurrence rate. Older studies describe a recurrence rate as<br />
high as 29 percent (Walshaw, 2976) as well as a 17 percent complication rate (Fox 1985)<br />
including premature dislodging of a tube, peritonitis, subcutaneous cellulites and persistent<br />
stoma drainage.<br />
Advantages of the incisional gastropexy are that 1) the procedure is rapidly done, 2) the stomach<br />
lumen is not entered and 3) fibrous connective tissue enters the abdominal rectus muscle and<br />
stomach wall to form a strong mature adhesion. The potential disadvantage is that the gaseous<br />
decompression is not provided in the postoperative period. The incisional gastropexy is popular<br />
among many North American surgeons but unfortunately no good retrospective studies are<br />
available to determine its clinical efficacy.<br />
The circumcostal technique has become popular for use in academic medicine because it<br />
probably forms a stronger adhesion. It is reported to be more difficult to perform than the other<br />
techniques but the author disagrees with this statement. Potential advantages include a 1) viable<br />
muscle flap adhesion as well as 2) a more proper anatomic placement of the stomach. Potential<br />
disadvantages include a prolonged surgical time, potential for rib fracture and potential for<br />
pneumothorax because of the close proximity to the diaphragm. Lieb (1984) reported on 39 dogs<br />
with circumcostal gastropexies to have a slightly lower recurrent rate (2.6 percent at 13.7<br />
months) than dogs with tube gastrostomy.<br />
Belt loop gastropexy offers similar advantages to the circumcostal and incisional gastropexies in<br />
that the gastric lumen is not entered and the risk of peritonitis is minimal. The technique is<br />
easily performed by an unassisted surgeon. Although the belt loop gastropexy has not been<br />
evaluated biomechanically one would suspect that breaking strengths would be superior to<br />
incisional or tube gastrostomy techniques but not quite as secure as circumcostal techniques<br />
since the base of the flap is narrower than the latter technique.<br />
<strong><br />
Postoperative Management</strong><br />
Diligent postoperative care is mandatory for successful outcome of the gastric dilatation volvulus<br />
patient. Most dogs that die in the postoperative period will do so within the first 3-4 days after<br />
surgery. After major gastric resection the animal is kept NPO for a period of 24-48 hours.<br />
Maintenance fluid, electrolyte and acid base status is critical during this period. Maintenance<br />
fluid should be given at a rate of 40-60 ml/kg per day. Although many dogs maintain normal<br />
serum potassium levels following gastric dilatation volvulus a total body potassium deficit may<br />
exist because of the NPO status, vomiting, oral gastric innervation and removal of gastric<br />
secretions. Therefore, supplementation of 20 mEq of potassium chloride is usually added to each<br />
liter of fluids to help maintain a total body potassium. Hypokalemia can also contribute to the<br />
development of cardiac arrhythmias, and gastrointestinal ilius.<br />
<strong><br />
The Role of Reperfusion in GDV</strong><br />
Mortality associated with gastric dilatation volvulus is most often due to gastrointestinal<br />
ischemia secondary to the large twisted stomach. It has been estimated that mortality can<br />
increase to 60 percent in the presence of gastric necrosis. Tissue ischemia to the gastric wall<br />
occurs due to reductions in arterial perfusion and venous stasis within the stomach wall. When<br />
the stomach is decompressed via the stomach tube and derotated via surgery there is rapid<br />
reperfusion of this ischemic tissue. Paradoxically, tissue ischemia followed by reperfusion with<br />
oxygenated blood may further increase tissue damage due to a phenomenon known as<br />
reperfusion injury.<br />
Reperfusion injury is thought to be mediated through the activity of oxygen-derived free radicals<br />
that is based on an iron dependent mechanism. These free radicals result in cellular lipid<br />
peroxidation and cell death. Since GDV is associated with high mortality and since most deaths<br />
occur within 96 hours of surgical intervention it is plausible that treatment directed toward<br />
preventing or moderating reperfusion injury may improve survival following the correction of<br />
GDV. Studies in experimental dogs with GDV have shown that xanthene oxidase inhibitors<br />
such as allopurinol and iron chelators such as deferoxamine have been helpful in reducing the<br />
amount of free radical production consequently minimizing cellular damage due to reperfusion<br />
injury and potentially decreasing mortality associated with GDV. Although experimental results<br />
are preliminary, it is likely that within five years some of these now experimental drugs will be<br />
utilized in emergency centers for the clinical management of GDV.</p>
<p>Bloat Risk Ranking for 24 Purebreeds, Compared with Risk for All Dogs Combined *</p>
<p><!-- 		@page { size: 8.5in 11in; margin: 0.79in } 		TD P { margin-bottom: 0in } 		P { margin-bottom: 0.08in } --></p>
<table style="height: 25px;" border="1" cellspacing="0" cellpadding="4" width="577" bordercolor="#000000">
<col width="108*"></col>
<col width="40*"></col>
<col width="55*"></col>
<col width="53*"></col>
<tbody>
<tr valign="TOP">
<td width="42%"><strong>Breed </strong></td>
<td width="16%"><strong>Affected</strong></td>
<td width="22%"><strong>Not Affected</strong></td>
<td width="21%"><strong>Risk Rank</strong></td>
</tr>
</tbody>
</table>
<p><!-- 		@page { size: 8.5in 11in; margin: 0.79in } 		TD P { margin-bottom: 0in } 		P { margin-bottom: 0.08in } --></p>
<table border="1" cellspacing="0" cellpadding="4" width="100%" bordercolor="#000000">
<col width="108*"></col>
<col width="40*"></col>
<col width="55*"></col>
<col width="53*"></col>
<tbody>
<tr valign="TOP">
<td width="42%"><strong><br />
</strong></p>
<p>Great Dane†</p>
<p>St. Bernard†</p>
<p>Weimaraner†</p>
<p>Irish Setter†</p>
<p>Gordon Setter†</p>
<p>Standard Poodle†</p>
<p>Basset Hound†</p>
<p>Doberman Pinscher†</p>
<p>Old English Sheepdog</p>
<p>German Shorthaired Pointer</p>
<p>Newfoundland</p>
<p>Airedale Terrier</p>
<p>German Shepherd Dog†</p>
<p>Alaskan Malamute</p>
<p>Chesapeake Bay Retriever</p>
<p>Boxer</p>
<p>Collie</p>
<p>Labrador Retriever</p>
<p>English Springer Spaniel</p>
<p>Samoyed</p>
<p>Dachshund</p>
<p>Golden Retriever‡</p>
<p>American Cocker Spaniel</p>
<p>Miniature Poodle‡</td>
<td width="16%"><strong><br />
</strong></p>
<p>299</p>
<p>81</p>
<p>49</p>
<p>180</p>
<p>24</p>
<p>47</p>
<p>39</p>
<p>139</p>
<p>27</p>
<p>25</p>
<p>13</p>
<p>12</p>
<p>202</p>
<p>23</p>
<p>10</p>
<p>28</p>
<p>39</p>
<p>72</p>
<p>18</p>
<p>13</p>
<p>26</p>
<p>37</p>
<p>14</p>
<p>10</td>
<td width="22%"><strong><br />
</strong></p>
<p>37</p>
<p>19</p>
<p>13</p>
<p>65</p>
<p>10</p>
<p>33</p>
<p>34</p>
<p>130</p>
<p>29</p>
<p>28</p>
<p>15</p>
<p>15</p>
<p>246</p>
<p>29</p>
<p>14</p>
<p>39</p>
<p>71</p>
<p>182</p>
<p>45</p>
<p>42</p>
<p>81</p>
<p>158</p>
<p>115</p>
<p>159</td>
<td width="21%"><strong><br />
</strong></p>
<p>1</p>
<p>2</p>
<p>3</p>
<p>4</p>
<p>5</p>
<p>6</p>
<p>7</p>
<p>8</p>
<p>9</p>
<p>10</p>
<p>11</p>
<p>12</p>
<p>13</p>
<p>14</p>
<p>15</p>
<p>16</p>
<p>17</p>
<p>18</p>
<p>19</p>
<p>20</p>
<p>21</p>
<p>22</p>
<p>23</p>
<p>24</td>
</tr>
</tbody>
</table>
<p>*Rank based on unadjusted odds ration (an estimate of relative risk) in purebreeds for which<br />
there were &gt; ten cases and &gt; eight controls. All dogs combined (pure and mixed breeds)<br />
included 1934 cases and 3868 controls.<br />
†Risk significantly higher than for all dogs combined.<br />
‡Risk significantly lower than for all dogs combined.<br />
From Glickman LT2. Epidemiologic Studies on Bloat in Dogs. Purina Veterinary Previews,<br />
1992; 2: 10-15.<br />
References<br />
1) Glickman LT, Glickman NW, Shellenburg DB, et al.: Multiple risk factors for the gastric<br />
dilation volvulus syndrome in dogs: A practitioner/owner case control study. J Am Anim<br />
Hosp Assoc 33: 197-204, 1997.<br />
2) Glickman LT, Glickman NW, Shellenburg DB, et al.: Epidemiologic studies of bloat in<br />
dogs. Purina Veterinary Previews 2: 10-15, 1997.<br />
3) Badylak SF, Lantz GC, Jeffires M: Prevention of reperfusion injury in surgically induced<br />
gastric dilatation volvulus in dogs. Am J Vet Res 51:294-299, 1990.<br />
4) Ellison GW: Gastric dilatation volvulus: Surgical prevention. Vet Clinics N Am 27: 513-<br />
521, 1993.<br />
5) Glickman LT. Epidemiology of gastric dilatation-volvulus in dogs. Waltham Focus 7:9-<br />
11, 1997.</p>
<p>Dog Owners and Breeders Symposium<br />
July 28, 2001<br />
University of Florida<br />
College of Veterinary Medicine</p>
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		<title>Influence of barometric pressure on GDV (bloat)</title>
		<link>http://webcanine.com/2010/influence-of-barometric-pressure-on-gdv-bloat/</link>
		<comments>http://webcanine.com/2010/influence-of-barometric-pressure-on-gdv-bloat/#comments</comments>
		<pubDate>Sun, 05 Sep 2010 21:30:19 +0000</pubDate>
		<dc:creator>mom</dc:creator>
				<category><![CDATA[Bloat (GDV)]]></category>
		<category><![CDATA[bloat]]></category>
		<category><![CDATA[gdv]]></category>

		<guid isPermaLink="false">http://webcanine.com/?p=1066</guid>
		<description><![CDATA[<p>Abstract:</p>
<p>Gastric dilatation-volvulus (GDV) is a life-threatening condition in dogs and other species in which the stomach dilates and rotates on itself. The etiology of the disease is multi-factorial, but explicit precipitating causes are unknown. This study sought to determine if there was a significant association between changes in hourly-measured temperature and/or atmospheric pressure and the occurrence <span style="color:#777"> . . . &#8594; Read More: <a href="http://webcanine.com/2010/influence-of-barometric-pressure-on-gdv-bloat/">Influence of barometric pressure on GDV (bloat)</a></span>]]></description>
			<content:encoded><![CDATA[<p><strong>Abstract:</strong></p>
<p>Gastric dilatation-volvulus (GDV) is a life-threatening condition in dogs and other species in which the stomach dilates and rotates on itself. The etiology of the disease is multi-factorial, but explicit precipitating causes are unknown. This study sought to determine if there was a significant association between changes in hourly-measured temperature and/or atmospheric pressure and the occurrence of GDV in the population of high-risk working dogs in Texas. The odds of a day being a GDV day, given certain temperature and atmospheric pressure conditions for that day or the day before, was estimated using logistic regression models. There were 57 days in which GDV(s) occurred, representing 2.60% of the days in the 6-year study period. <em>The months of November, December, and January collectively accounted for almost half (47%) of all cases</em>. Disease risk was negatively associated with daily maximum temperature. An increased risk of GDV was weakly associated with the occurrence of large hourly drops in temperature that day and of higher minimum barometric pressure that day and the day before GDV occurrence, but extreme changes were not<br />
predictive of the disease.</p>
<p><a href="http://webcanine.com/wp-content/uploads/2010/08/GDV_biometeor.pdf" target="_blank">pdf</a></p>
]]></content:encoded>
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		<title>Parvo puppy diarrhea treatment</title>
		<link>http://webcanine.com/2007/parvo-puppy-diarrhea-treatment/</link>
		<comments>http://webcanine.com/2007/parvo-puppy-diarrhea-treatment/#comments</comments>
		<pubDate>Mon, 17 Sep 2007 22:25:09 +0000</pubDate>
		<dc:creator>mom</dc:creator>
				<category><![CDATA[Gastro-Intestinal]]></category>
		<category><![CDATA[parvo]]></category>
		<category><![CDATA[parvo treatment]]></category>

		<guid isPermaLink="false">http://webcanine.com/2007/parvo-puppy-diarrhea-treatment/</guid>
		<description><![CDATA[<p>Canine IGY Plus Gel</p>
<p>A direct fed microbial gel for Dogs and Puppies containing a source of live, naturally occurring microorganisms, pasteurized dried egg product, vitamins and antioxidants</p>
<p>For support of digestive sytem disturbances</p>
<p>PRN Canine IgY Plus Gel is a highly palatable flavored gel intended for use in both dogs and puppies. Manufactured with dried egg product and <span style="color:#777"> . . . &#8594; Read More: <a href="http://webcanine.com/2007/parvo-puppy-diarrhea-treatment/">Parvo puppy diarrhea treatment</a></span>]]></description>
			<content:encoded><![CDATA[<p>Canine IGY Plus Gel</p>
<p>A direct fed microbial gel for Dogs and Puppies containing a source of live, naturally occurring microorganisms, pasteurized dried egg product, vitamins and antioxidants</p>
<p><font color="#ff0000">For support of digestive sytem disturbances</font></p>
<p><em>PRN Canine IgY Plus Gel </em>is a highly palatable flavored gel intended for use in both dogs and puppies. Manufactured with dried egg product and direct fed microbials, antioxidants and vitamins, <em>Canine IgY Plus</em> supports treatment for digestive system disturbances of known or unknown origin with the highest viral antibody titers in the industry. Developed from cutting-edge technology, <em>Canine IgY Plus</em> also can help puppies bridge over the “blank period” between natural local immunity and vaccination.<br />
<span id="more-141"></span><br />
The dried egg product in <em>Canine IgY Plus</em> is characterized by the content of yolk antibodies (IgY immunoglobulin) to microbial agents which can cause disorders in the normal state of the digestive tract, impair physiological digestive functions and affect rearing of pups as well as the general state of health and performance of adult dogs.</p>
<p>The dried egg product is prepared exclusively of eggs laid by hens which have been subjected to specific immunization programs. The egg mass contains antibodies to the most important enteropathogenic agents.</p>
<p>In the canine intestinal tract, these antibodies bind to the surface of canine <em>parvovirus, coronavirus, rotavirus salmonella</em> and <em>E. coli</em> cells creating an antigen-antibody complex in the G.I. tract which prevents the antigen from adhering to the intestinal mucosa and establishing in the intestinal contents. The antibodies enhance the efficacy and/or help bridge the insufficiency of the natural local immunity. Dried egg product, the major component of <em>Canine IgY Plus,</em> contains easily digestible proteins with high nutritional values.</p>
<p>No component of <em>Canine IgY Plus</em> influences the chemical composition or efficacy of drugs used in the treatment of canine intestinal disturbances. <em>PRN Canine IgY Plus</em> does not affect drug activity in the digestive tract, absorption into the blood circulation nor distribution and activity in the organism. This applies to antibiotics as well as other drugs which may be deemed desirable for treatment by the veterinarian.</p>
<p><strong>Guaranteed Analysis:</strong>  Every 3 cc&#8217;s contains a minimum of 2 Billion CFU&#8217;s of total Lactic Acid &#8211; Producing Bacteria (Enterococcus faecium, Lactobacillus Acidophilus, Bacillus Subtilis, Bacillus Pumilis, Bifidobacterium Bifidum), .3 Billion CFU&#8217;s of live yeast (Saccharomyces), .75 gm. of pasteurized sprayed dried egg product. .5 gm. Fructooligosaccharides, 75 mg. Ascorbic Acid, and 45 mg. Vitamin E</p>
<p><strong>Ingredients: </strong>Atlantic Salmon Oil containing Omega 3, Liver Flavoring, Dried Enterococcus faecium Fermentation product, Dried Lactobacillus Acidophilus, Bacillus Subtilis, Bacillus Pumilis, Bifidobacterium Bifidum Fermentation product, Sprayed Egg Product, Fructooligosaccharides, Ascorbic Acid and Vitamin E</p>
<p><em>Canine IgY Plus Gel</em> contains <strong>2 billion CFU&#8217;s of LAB</strong>, including live cultures of <em>Enterococcus faecium</em>, <em>Lactobacillus acidophilus, Bacillus subtilis, Bacillus pumilus</em> and <em>Bifidobacterium bifidum</em> which propagate rapidly in the canine digestive tract and support growth of other symbiotic intestinal microorganisms. It contains live yeast as well, specifically <em>Saccharomyces cerevisiae</em> (1 Billion cfu&#8217;s in 3 cc. Yeast cell walls contain -glucans which are proposed to enhance immune system function.</p>
<ul>
<li><em>Bacillus </em>strains are known for optimizing food utilization.</li>
<li><em>Bifidobacterium bifidum</em> is critical for aiding young animals in the production of LAB and producing enzymes for cell development and cell repair.</li>
<li>Omega 3 fatty acids derived from Atlantic Salmon Oil enhance the immune system and produce anti-inflammatory effects by counterbalancing the pro-inflammatory prostaglandins (PG2) and limiting the secretion of PG2 at the cellular level which reduces pro-inflammatory allergic responses.</li>
</ul>
<p><em>Fructo-oligosaccharide</em> (FOS) is a natural source of inulin, a carbohydrate made up of fructose polymers. The FOS cannot be metabolized by monogastics, which lack the enzyme inulinase. The FOS passes to the lower intestine where it is fermented by LAB such as <em>Bifidobacterium.</em> Gram negative bacteria, such as <em>Escherichia coli (E. coli</em>), are unable to grow on FOS; this creates a natural selection process which promotes beneficial bacteria in the lower intestine.</p>
<p><a href="http://www.vetproductforum.com/4-45/index.html">http://www.vetproductforum.com/4-45/index.html<</p>
]]></content:encoded>
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		<title>Med-surgical treatment for bloat</title>
		<link>http://webcanine.com/2007/med-surg-treatment-for-bloat/</link>
		<comments>http://webcanine.com/2007/med-surg-treatment-for-bloat/#comments</comments>
		<pubDate>Mon, 30 Apr 2007 23:37:44 +0000</pubDate>
		<dc:creator>mom</dc:creator>
				<category><![CDATA[Bloat (GDV)]]></category>
		<category><![CDATA[bloat]]></category>
		<category><![CDATA[gdv]]></category>

		<guid isPermaLink="false">http://webcanine.com/beta/2007/med-surg-treatment-for-bloat/</guid>
		<description><![CDATA[<p>Bloat is a life-threatening, acute emergency prepare a bloat kit (google search for bloat kit to choose one), print out this article to keep in a safe place and in your car, to take to the ER vet. Know the symptoms of bloat.</p>
<p align="left">Medical and Surgical Considerations Regarding Bloat        <span style="color:#777"> . . . &#8594; Read More: <a href="http://webcanine.com/2007/med-surg-treatment-for-bloat/">Med-surgical treatment for bloat</a></span>]]></description>
			<content:encoded><![CDATA[<p>Bloat is a life-threatening, acute emergency prepare a bloat kit (google search for bloat kit to choose one), print out this article to keep in a safe place and in your car, to take to the ER vet. Know the symptoms of bloat.</p>
<p align="left"><span id="more-107"></span><strong>Medical and Surgical Considerations Regarding Bloat          Gastric Dilatation Volvulus Syndrome in the Bloodhound </strong></p>
<p align="left">Dr. John Hamil</p>
<p align="left">Of the approximately 1,300,000 dogs registered annually by the AKC only 1500 are bloodhounds. Consequently, most veterinarians will see only a few in their practice lifetime</p>
<p>This brochure is offered by the American Bloodhound Club in an attempt to educate the owners of bloodhounds about the life-threatening nature of this complex syndrome as well as to familiarize veterinarians with some of the peculiarities of our breed and a protocol which has been employed successfully in treating GDV syndrome.</p>
<p align="left"> Definition: this is an acute life-threatening condition which initiates complex cardiovascular and metabolic changes that result in high mortality following dilatation and rotation of the stomach on its long axis.</p>
<p align="left">CONCERN: Early recognition of the signs of GDV and immediate veterinary attention will greatly improve survival rate. Only if veterinary care is not accessible should the owner attempt to tube or trocarize the dog, although this may be life saving if you must travel a great distance.</p>
<p align="left">CAUSE: Unkown. Probably multifactorial. No age or sex predilection. The bloodhound&#8217;s size, deep chest, frequent ingestion of foreign material, and genetic predisposition make them common victims of this condition. GDV syndrome is seen primarily in large deep chested breeds and, although heritability has not been proven, does seem to be more prevalent in certain lines. This syndrome is often associated with ingestion of large meals and drinking water, post feeding exercise, following general anesthesia, stress (boarding, traveling, showing, breeding, trailing, etc.) ingestion of foreign bodies, and gastroenteritis with vomition.</p>
<p align="left"><strong>SIGNS: The observant owner may notice the early vague signs of restlessness, pacing, lethargy, dull, vacant or painful expression, and/or shallow respiration. Repeated measurements around the abdomen at the level of the last rib with a cloth measuring tape will demonstrate early increases in abdominal size if you are in doubt. Every owner should be able to recognize the more sever signs of unresponsiveness, unproductive retching, salivation, arched back, anterior abdominal pain, abdominal distention, abdominal tenseness, pale mucus membranes (eyes and mouth), weak pulse, blue-gray mucus membranes, weakness, inability to stand, moribund appearance, and, with endotoxic shock, red injected mucus membranes and rapid capillary refill time.</strong></p>
<p align="left">RULE OUTS: Small intestinal volvulus, splenic torsion, gastric or intestinal foreign body, intussesception, peritonitis, cardiomyopathy, or pleural effusion. Bloodhounds are predisposed to both dilated and hypertrophic cardiomyopathy. They are very likely to ingest foreign objects and seem to be susceptible to intussusception.</p>
<p align="left">DIAGNOSIS: Signalment, history, clinical signs, xray in right lateral recumbency if not in shock or after decompression, this position may show the pylorus and duodenum dorsal to the cardia.</p>
<p align="left">THERAPY: If in shock, decompress immediately by gastric tube, or if necessary, by trocharization with multiple 16-18 gauge needles at the point of greatest distention or perform temporary gastrostomy in right paracostal area, if necessary. If possible have assistants establish IV and initiate treatment for shock simultaneously. If assistant is not available, decompress first, then follow remainder of protocol.</p>
<p align="left"> If not in shock try to pass lubricated stomach tube marked at distance from nose to last rib. If unable to pass stomach tube, stand dog on rear legs and &#8220;bounce&#8221; up and down. if still unable to pass tube in sitting position, trocarize, if still unsuccessful take to surgery immediately after establishing IV and administering medication.</p>
<p align="left">* start IV LRS (50 cc/lb rapid IV infusion for first hour)</p>
<p align="left">* place IV catheter (multiple if needed for severe shock)</p>
<p align="left">* give corticosteroids (500 mg Soludelta cortef IV) for endotoxic    shock</p>
<p align="left"> * flunixin meglumine (one time 0.5 mg/lb IV) for endotoxic shock</p>
<p align="left">* gentamycin (1 mg/lb) or cephalothin sodium (10 mg/lb) in initial    fluids</p>
<p align="left"> * sodium bicarbonate (2 meq/lb in initial fluids) if suspect    metabolic acidosis</p>
<p align="left">* metoclopramide (10 mg SQ) improves gastric emptying and antiemetic</p>
<p align="left"> * ranitidine (1 mg/lb IV every 8 hours)</p>
<p align="left"> * start ECG and cardiac medications (60 mg lidocaine in initial fluids) for expected arrhythmias, give additional lidocaine as needed (1 mg/lb IV bolus)</p>
<p align="left">* pass stomach tube and lavage stomach removing all content, give coative with simethicone. Take to surgery as soon as possible, particularly if digested blood or mucosal shreds are found in stomach content.</p>
<p align="left"> Monitor intensively for cardiac complications until surgery, usually within 4-6 hours, some surgeons prefer to wait until the next day. When stable, hopefully with cardiac signs normal, perform permanent abdominal wall gastropexy. Although patient is not as critical at this time, all precautions must be taken:</p>
<p align="left"> * Add 60 mg of lidocaine to initial fluids</p>
<p align="left">* Induce anesthesia with Propofol, Numorphan, Ket/Val, etc. (no    barbiturates or nitrous oxide)</p>
<p align="left"> * Intubate and inflate cuff</p>
<p align="left">* Maintain on isoflurane or halothane 1-2 %</p>
<p align="left">* Lead 2 EKG monitoring</p>
<p align="left">* Careful on incising linea due to presence of distended stomach    or spleen</p>
<p align="left">* If markedly distended, decompress stomach with 16-18 gauge needle    and suction before trying to derotate</p>
<p align="left"> * Remember stomach usually rotates from right to left with pylorus passing ventrally to rest dorsally on left side above the cardia. Always determine position prior to derotation and be gentle, as stomach wall may be friable particularly on greater curvature near cardia. Standing on the right side of the patient in dorsal recumbency, reach across the stomach and elevate the pylorus while pushing the body of the stomach down and away from you, thereby reducing the usual clockwise rotation. If devitalized, excise and close with a 2-layer inverting pattern with 2-0 PDS. Try not to open stomach if it can be avoided.</p>
<p align="left">* have assistant pass stomach tube, empty and lavage stomach</p>
<p align="left">. * Inspect spleen for infraction or thrombosed vessels. Splenectomy    if necessary. Always ligate close to spleen.</p>
<p align="left">* Permanent abdominal wall gastropexy (Circumcostal, belt loop,    or muscle flap).</p>
<p align="left">* Inspect abdomen. Look for torsed intestinal mesenteries. Resect    if necessary.</p>
<p align="left">* Standard abdominal closure.</p>
<p align="left">* Continue cardiac monitoring post operatively until fully recovered from anesthesia. If lidocaine drip fails to control VPC&#8217;s:</p>
<p align="left">* Give 3-10 mg/lb quinidine deep IM</p>
<p align="left"> * Give 375 mg oral pronestyl every 6 hours</p>
<p align="left"> * May need 500 mg oral Procan-S-R every 8 hours If patient experiences    tachycardia with rate over 200 bpm</p>
<p align="left">* Give 1/2 mg Inderal IV and monitor return to normal rate. Can repeat as needed up to 3 mg total dose. POST-OP: * NPO for 12 hours</p>
<p align="left">* Tepid water and warm ID gruel tid for 4-5 days, should eat within 24 hours, if not suspect ileus, possibly due to intussesception.</p>
<p align="left">* Canned ID or dry ID soaked in warm water</p>
<p align="left">* 500 mg oral Keflex bid for 7 days</p>
<p align="left">* 10 mg oral cisapride bid for 3 days (same effects as metoclopramide except not antiemetic plus stimulates motility in small and large intestine)</p>
<p align="left">* Antiarrhythmic drugs as needed tapered in 7-10 days</p>
<p align="left"> * Recheck, including EKG in 7 days</p>
<p align="left">* Sutures out at 10-14 days</p>
<p align="left">PREVENTION:</p>
<p align="left">* Feed 2-4 times daily</p>
<p align="left"> * Soak dry kibble in hot water for 5-10 minutes prior to feeding</p>
<p align="left">* Limit exercise and water consumption for one hour after eating</p>
<p align="left"> * Prophylactic gastropexy if relatives have been affected (disadvantage    in trying to evaluate breeding potential)</p>
<p align="left">* Add simethicone to food<</p>
]]></content:encoded>
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		<title>Irritable bowel disease</title>
		<link>http://webcanine.com/2007/irritable-bowel-disease/</link>
		<comments>http://webcanine.com/2007/irritable-bowel-disease/#comments</comments>
		<pubDate>Wed, 25 Apr 2007 03:07:54 +0000</pubDate>
		<dc:creator>mom</dc:creator>
				<category><![CDATA[Gastro-Intestinal]]></category>
		<category><![CDATA[ibd]]></category>
		<category><![CDATA[ibs]]></category>

		<guid isPermaLink="false">http://webcanine.com/beta/2007/irritable-bowel-disease/</guid>
		<description><![CDATA[<p>IBD has been defined clinically as a spectrum of gastrointestinal disorders associated with chronic inflammation of the stomach, intestine and/or colon of unknown pathogenesis and etiology.</p>
<p align="center">Canine I.B.D. – Pathogenesis, Diagnosis, and Therapy</p>
<p align="center">Treatment with Flagyl</p>
<p> Etiology &#8211; Inflammatory bowel disease (IBD) has been defined on the basis    of clinical, histologic, immunologic, pathophysiologic, <span style="color:#777"> . . . &#8594; Read More: <a href="http://webcanine.com/2007/irritable-bowel-disease/">Irritable bowel disease</a></span>]]></description>
			<content:encoded><![CDATA[<p>IBD has been defined clinically as a spectrum of gastrointestinal disorders associated with chronic inflammation of the stomach, intestine and/or colon of unknown pathogenesis and etiology.<span id="more-50"></span></p>
<p align="center"><strong>Canine I.B.D. – Pathogenesis, Diagnosis, and Therapy</strong></p>
<p align="center"><strong><a href="http://www.webcanine.com/flagyl.htm">Treatment with Flagyl</a></strong></p>
<p> Etiology &#8211; Inflammatory bowel disease (IBD) has been defined on the basis    of clinical, histologic, immunologic, pathophysiologic, and genetic criteria.</p>
<p><strong>Clinical Definition of IBD</strong></p>
<p>IBD has been defined clinically as a spectrum of gastrointestinal disorders    associated with chronic inflammation of the stomach, intestine and/or colon    of unknown pathogenesis and etiology. A clinical diagnosis of IBD is considered    only if affected animals have persistent (&gt;3 weeks in duration) gastrointestinal    signs (anorexia, vomiting, weight loss, diarrhea, hematochezia, mucousy feces),    failure to respond to dietary (novel protein, hydrolyzed-, anti-oxidant-, or    highly digestible diets) or symptomatic therapies (parasiticides, antibiotics,    gastrointestinal protectants) alone, failure to document other causes of gastroenterocolitis    by thorough diagnostic evaluation, and histologic diagnosis of benign intestinal    inflammation (Jergens et al., 2003). Small bowel and large bowel forms of IBD    have been reported in both dogs and cats, although large bowel IBD appears to    be more prevalent in the dog.</p>
<p><strong>Histologic Definition of IBD</strong></p>
<p>IBD has been defined histologically by the type of inflammatory infiltrate    (neutrophilic, eosinophilic, lymphocytic, plasmacytic, granulomatous), associated    mucosal pathology (villus atrophy, fusion, crypt collapse), distribution of    the lesion (focal or generalized, superficial or deep), severity (mild, moderate,    severe), mucosal thickness (mild, moderate, severe), and topography (gastric    fundus, gastric antrum, duodenum, jejunum, ileum, cecum, ascending colon, descending    colon). As with small intestinal IBD, the histologic assessment of large intestinal    IBD lesions has been fraught with subjective interpretations. The lack of objective    morphologic criteria has made it difficult to compare tissue findings between    pathologists. Subjectivity in histologic assessments have led to the development    of IBD grading systems (van der Gaag, 1988; van der Gaag, 1989; Spinato et al.,    1990; Roth et al., 1990, Roth et al., 1992; Wilcock, 1992; Leib et al., 1992;    Stonehewer et al., 1998). In more recent times, pathologists and internists    are increasingly emphasizing architectural changes (villus atrophy, villus fusion,    fibrosis) instead of lamina proprial cellularity.</p>
<p><strong>Immunologic Definition of IBD</strong></p>
<p>IBD has been defined immunologically by the innate and adaptive response of    the mucosa to gastrointestinal antigens. Although the precise immunologic events    of canine IBD remain to be determined, a prevailing hypothesis for the development    of IBD is the loss of immunologic tolerance to the normal bacterial flora or    food antigens, leading to abnormal T cell immune reactivity in the gut microenvironment.    Genetically engineered animal models (e.g., IL-2, IL-10, and T cell receptor    knockouts) that develop IBD involve alterations in T cell development and/or    function suggesting that T cell populations are responsible for the homeostatic    regulation of mucosal immune responses. Immunohistochemical studies of canine    IBD have demonstrated an increase in the T cell population of the lamina propria,    including CD3+ cells and CD4+ cells, as well as macrophages, neutrophils, and    IgA-containing plasma cells. Many of the immunologic features of canine IBD    can be explained as an indirect consequence of mucosal T cell activation. Enterocytes    are also likely involved in the immunopathogenesis of IBD. Enterocytes are capable    of behaving as antigen-presenting cells, and interleukins (e.g., IL-7 and IL-15)    produced by enterocytes during acute inflammation activate mucosal lymphocytes.    Up-regulation of Toll-like receptor 4 (TLR4) and Toll-like receptor 2 (TLR2)    expression contribute to the innate immune response of the colon. Thus, the    pathogenesis and pathophysiology of IBD appears to involve the activation of    a subset of CD4+ T cells within the intestinal epithelium that overproduce inflammatory    cytokines with concomitant loss of a subset of CD4+ T cells, and their associated    cytokines, which normally regulate the inflammatory response and protect the    gut from injury. Enterocytes, behaving as antigen-presenting cells, contribute    to the pathogenesis of this disease (Carding et al.).</p>
<p><strong>Pathophysiologic Definition of IBD</strong></p>
<p>IBD may be defined pathophysiologically in terms of transport, blood flow,    and motility abnormalities. The clinical signs of IBD, whether small or large    bowel, have long been attributed to the pathophysiology of malabsorption and    hypersecretion, but experimental models of canine IBD have instead related clinical    signs to the emergence of abnormality motility patterns..</p>
<p><strong>Genetic Definition of IBD</strong></p>
<p>IBD may be defined in genetic terms in several animal species. Crohn’s    disease and ulcerative colitis are more common in certain human genotypes, and    a mutation in the NOD2 gene (nucleotide-binding oligomerization domain2) has    been found in a sub-group of patients with Crohn’s disease (Strober). Genetic    influences have not yet been identified in canine or feline IBD, but certain    breeds (e.g., German shepherd, Boxers) appear to be at increased risk for the    disease.</p>
<p><strong>Pathophysiology</strong></p>
<p>The pathophysiology of colitis-type IBD is explained by at least two interdependent    phenomena: the mucosal immune response, and associated changes in motility.</p>
<p><strong>Immune Responses</strong></p>
<p>A generic inflammatory response involving cellular elements (B and T lymphocytes,    plasma cells, macrophages, and dendritic cells), secretomotor neurons (e.g.,    VIP, substance P, and cholinergic neurons), cytokines and interleukins, and    inflammatory mediators (e.g., leukotrienes, prostanoids, reactive oxygen metabolites,    nitric oxide, 5-HT, IFN-? TNF-? and platelet-activating factor) is typical of    canine and feline inflammatory bowel disease. There are many similarities between    the inflammatory response of the small and large intestine, but recent immunologic    studies suggest that IBD of the canine small intestine is a mixed Th1/Th2 response    (German et al. 2001) whereas IBD of the canine colon may be more of a Th1 type    response with elaboration of IL-2, IL-12, INF-?, and TNF-a (Ridyard et al. 2001).    Other studies of canine colonic IBD have demonstrated increased numbers of mucosal    IgA- and IgG-containing cells, CD3+ T cells, nitric oxide (NO), and inducible    nitric oxide synthase (iNOS) in the inflamed colonic mucosa. Increases in the    CD3+ positive T cell population of the inflamed colon are consistent with increases    previously reported in the inflamed canine small intestine. Thus, there are    important similarities and differences between small and large bowel IBD.</p>
<p><strong>Motility Changes</strong></p>
<p>Experimental studies of canine IBD have shown that many of the clinical signs    (diarrhea, passage of mucus and blood, abdominal pain, tenesmus, and urgency    of defecation) are related to motor abnormalities of the colon. Ethanol and    acetic acid perfusion of the canine colon induces a colitis-type IBD syndrome    indistinguishable from the natural condition (Sethi and Sarna, 1991). Inflammation    in this model suppresses the normal phasic contractions of the colon, including    the migrating motility complex, and triggers the emergence of giant migrating    contractions (GMCs). The appearance of these GMCs in association with inflammation    is a major factor in producing diarrhea, abdominal cramping, and urgency of    defecation. GMCs are powerful lumen-occluding contractions that rapidly propel    pancreatic, biliary, and intestinal secretions in the fasting state, and undigested    food in the fed state, to the colon to increase its osmotic load (Sethi and    Sarna, 1991). Malabsorption results from direct injury to the epithelial cells    and from ultrarapid propulsion of intestinal contents by giant migrating contractions    (GMCs) so that sufficient mucosal contact time is not allowed for digestion    and absorption to take place.</p>
<p>Inflammation impairs the regulation of the colonic motility patterns at several    levels, i.e., enteric neurons, interstitial cells of Cajal, and circular smooth    muscle cells. Inflammation-induced changes in the amplitude and duration of    the smooth muscle slow wave plateau potentials contribute to the suppression    of rhythmic phasic contractions (RPCs). These alterations likely have their    origin in structural as well as functional damage to the interstitial cells    of Cajal (Lu et al.). At the same time that inflammation suppresses the (RPCs),    inflammation sensitizes the colon to the stimulation of GMCs by the neurotransmitter    substance P. These findings suggest that SP increases the frequency of GMCs    during inflammation, and that selective inhibition of GMCs during inflammation    may minimize the symptoms of diarrhea, abdominal discomfort, and urgency of    defecation associated with these contractions.</p>
<p>Inflammation suppresses the generation of tone and phasic contractions in the    circular smooth muscle cells through multiple molecular mechanisms. Inflammation    shifts muscarinic receptor expression in circular smooth muscles from the M3    to the M2 subtype (Jadcherla et al.). This shift has the effect of reducing    the overall contractility of the smooth muscle cell. Inflammation also impairs    calcium influx and down-regulates the expression of the L-type calcium channel    (Liu et al.), which may be important in suppressing phasic contractions and    tone while concurrently stimulating GMCs in the inflamed colon. Changes in the    open-state probability of the large conductance calcium-activated potassium    channels (KCa) partially attenuate this effect (Lu et al.). Inflammation also    modifies the signal transduction pathways of circular smooth muscle cells. Phospholipase    A2 and protein kinase C (PKC) expression and activation are significantly altered    by colonic inflammation and this may partially account for the suppression of    tone and phasic contractions (Ali et al.). PKC a, ? and e isoenzyme expression    is down-regulated, PKC i and l isoenzyme expression is up-regulated, and the    cytosol-to-membrane translocation of PKC is impaired. To worsen matters, the    L-type calcium channel (already reduced in its expression) is one of the molecular    targets of PKC. Inflammation also activates the transcription factor NF-kB which    further suppresses cell contractility (Shi et al.)</p>
<p><strong>Clinical Examination</strong></p>
<p>The clinical signs of colitis-type IBD are those of a large-bowel type diarrhea,    i.e., marked increased frequency, reduced fecal volume per defecation, red blood    pigments and mucous in feces, and tenesmus. Anorexia, weight loss, and vomiting    are occasionally reported in animals with severe IBD of the colon or concurrent    IBD of the stomach and/or small intestine. Clinical signs usually wax and wane    in their severity. A transient response to symptomatic therapy may occur during    the initial stages of IBD. As the condition progresses, diarrhea gradually increases    in its frequency and intensity, and may become continuous. In some cases the    first bowel movement of the day may be normal or nearly normal, whereas successive    bowel movements are reduced in volume and progressively more urgent and painful.    During severe episodes, mild fever, depression, and anorexia may occur.</p>
<p>There does not appear to be any sex predilection, but age may be a risk factor    with IBD appearing more frequently in middle aged animals (mean age approximately    6 years with a range of 6 months to 20 years). German shepherd and Boxer dogs    are at increased risk for IBD, and pure-breed cats appear to be at greater risk.    Cats more often present with an upper gastrointestinal form of IBD, whereas    dogs are at risk for both small and large bowel IBD.</p>
<p>Physical examination is unremarkable in most cases. Thickened bowel loops may    be detected during abdominal palpation if the small bowel is concurrently involved.    Digital examination of the anorecturm may evoke pain or reveal irregular mucosa,    and blood pigments and mucous may be evident on the exam glove.</p>
<p><strong>Diagnosis</strong></p>
<p>Complete blood counts, serum chemistries, and urinalyses are often normal in    mild cases of large bowel IBD. Chronic cases may have one or more subtle abnormalities.    One review of canine and feline IBD reported several hematologic abnormalities    including mild anemia, leukocytosis, neutrophilia with and without a left shift,    eosinophilia, eosinopenia, lymphocytopenia, monocytosis, and basophilia (Jergens).    The same study reported several biochemical abnormalities including increased    activities of serum alanine aminotransferase and alkaline phosphatase, hypoalbuminemia,    hypoproteinemia, hyperamylasemia, hyperglobulinemia, hypokalemia, hypocholesterolemia,    and hyperglycemia. No consistent abnormality in the complete blood count or    serum chemistry has been identified.</p>
<p>A scoring index for disease activity in canine IBD was recently developed that    relates severity of clinical signs to serum acute-phase protein concentrations    (C-reactive protein, serum amyloid A – Jergens et al., 2003). The canine    IBD activity index (CIBDAI) assigns levels of severity to each of several gastroenterologic    signs (e.g., anorexia, vomiting, weight loss, diarrhea), and it appears to be    a reliable index of mucosal inflammation in canine IBD. Interestingly, both    the CIBDAI and serum concentrations of C-reactive protein (CRP) improve with    successful treatment, suggesting that serum CRP is suitable for the laboratory    evaluation of therapy in canine IBD. Other acute-phase proteins were less specific    than CRP. One important caveat that should be emphasized is that altered CRP    is not prima facie evidence of gastrointestinal inflammation. Concurrent infections    or other inflammatory conditions could cause an acute-phase response, including    CRP, in affected patients.</p>
<p>Treatment – The treatment of canine I.B.D. has eight components of therapy:    (1) Dietary Management, (2) Exercise, (3) Antibiotics, (4) Probiotics, (5) Anti-Diarrheal    Therapy, (6) Restoration of G.I. Motility, (7) Immunosuppressive Therapy, and    (8) Behavioral Modification.</p>
<p><strong>Dietary Management</strong></p>
<p>The precise immunologic mechanisms of canine and feline IBD have not yet been    determined, but a prevailing hypothesis for the development of IBD is the loss    of immunologic tolerance to the normal bacterial flora or food antigens. Accordingly,    dietary modification may prove useful in the management of canine and feline    IBD. Several nutritional strategies have been proposed including novel proteins,    hydrolyzed diets, anti-oxidant diets, medium chain triglyceride supplementation,    low fat diets, modifications in the omega-6/omega-3 (w-6/w-3) fatty acid ratio,    and fiber supplementation. Of these strategies, some evidence-based medicine    has emerged for the use of novel protein, hydrolyzed, and fiber-supplemented    diets.</p>
<p>Food sensitivity reactions were suspected or documented in 49% of cats presented    because of gastroenterologic problems (with or without concurrent dermatologic    problems) in a prospective study of adverse food reactions in cats. Beef, wheat,    and corn gluten were the primary ingredients responsible for food sensitivity    reactions in that study, and most of the cats responded to the feeding of a    chicken- or venison-based selected-protein diet for a minimum of 4 weeks. The    authors concluded that adverse reactions to dietary staples are common in cats    with chronic gastrointestinal problems and that they can be successfully managed    by feeded selected-protein diets. Further support for this concept comes from    studies in which gastroenterologic or dermatologic clinical signs were significantly    improved by the feeding of novel proteins.</p>
<p>Evidence is accruing that hydrolyzed diets may be useful in the nutritional    management of canine IBD. The conceptual basis of the hydrolyzed diet is that    oligopeptides are of insufficient size and structure to induce antigen recognition    or presentation. In one preliminary study, dogs with inflammatory bowel disease    showed significant improvement following the feeding of a hydrolyzed diet although    they had failed to respond to the feeding of a novel protein. Clinical improvement    could not be solely attributed to the hydrolyzed nature of the protein source    because the test diet had other modified features, i.e., high digestibility,    cornstarch rather than intact grains, medium chain triglycerides, and an altered    ratio of w-6 to w-3 polyunsaturated fatty acids. Additional studies will be    required to ascertain the efficacy of this nutritional strategy in the management    of IBD.</p>
<p>Fiber-supplemented diets may be useful in the management of irritable bowel    syndrome (IBS) in the dog. IBS is a poorly defined syndrome in the dog that    may or may not bear resemblance to IBS in humans. Canine IBS has been defined    as a chronic large-bowel type diarrhea without known cause and without evidence    of colonic inflammation on colonoscopy or biopsy. Dogs fulfilling these criteria    were successfully managed with soluble fiber (psyllium hydrophilic mucilloid)    supplementation of a highly digestible diet.<br />
<strong>Exercise</strong></p>
<p>Experimental IBD in the dog is accompanied by significant abnormalities in    the normal colonic motility patterns. Physical exercise has been shown to disrupt    the colonic MMCs and to increase the total duration of contractions that are    organized as non-migrating motor complexes during the fed state. Exercise also    induces GMCs, defecation, and mass movement in both the fasted and fed states.    The increased motor activity of the colon and extra GMCs that result from physical    exercise may aid in normal colonic motor function.</p>
<p><strong>Antibiotics</strong></p>
<p>Three types of antibiotics (tylosin, metronidazole, oxytetracycline) have been    used with some success for the management of small intestinal bacterial overgrowth    (SIBO) in dogs. SIBO has not been documented in cats, however, so it’s    not clear whether these antibiotics will be as useful in the management of chronic    diarrheal states. One study has shown a reduction in the indigenous microflora    and an increase in serum cobalamin and albumin concentrations in cats treated    with metronidazole.<br />
<strong>Probiotics</strong></p>
<p>Probiotics are living organisms with low or no pathogenicity that exert beneficial    effects (e.g., stimulation of innate and acquired immunity) on the health of    the host. The Gram-positive commensal lactic acid bacteria (e.g., Lactobacilli)    have many beneficial health effects, including enhanced lymphocyte proliferation,    innate and acquired immunity, and anti-inflammatory cytokine production. Lactobacillus    rhamnosus GG, a bacterium used in the production of yogurt, is effective in    preventing and treating diarrhea, recurrent Clostridia difficile infection,    primary rotavirus infection, and atopic dermatitis in humans. Lactobacillus    rhamnosus GG has been safely colonized in the canine gastrointestinal tract,    although probiotic effects in the canine intestine have not been firmly established.    The probiotic organism, Enterococcus faecium (SF68), has been safely colonized    in the canine gastrointestinal tract, and it has been shown to increase fecal    IgA content and circulating mature B (CD21+/MHC class II+) cells in young puppies.    It has been suggested that this probiotic may be useful in the prevention or    treatment of canine gastrointestinal disease. This organism may, however, enhance    Campylobacter jejuni adhesion and colonization of the dog intestine, perhaps    conferring carrier status on colonized dogs.</p>
<p>Two recent studies have shown that many commercial veterinary probiotic preparations    are not accurately represented by label claims. Quality control appears to be    deficient for many of these formulations. Until these products are more tightly    regulated, veterinarians should probably view product claims with some skepticism.</p>
<p><strong>Anti-Diarrheal Therapy</strong></p>
<p>Four major classes of anti-diarrheal agents are available for use in canine    I.B.D. These drugs directly inhibit crypt epithelial secretion or they directly    promote villus epithelial absorption.</p>
<p><strong>Prostaglandin Synthetase Inhibitors</strong></p>
<p>1. Sulfasalazine &#8211; 10-25 mg/kg TID-QID, PO</p>
<p>2. Olsalazine &#8211; 5-10 mg/kg PO, TID-QID (dog)</p>
<p><strong>Opioid Agonists</strong> – These drugs stimulate absorption, and inhibit    secretion of, fluid and electrolytes.</p>
<p>1. Loperamide 0.08 mg/kg TID, PO-preferred drug</p>
<p>2. Diphenoxylate 0.05-0.10 mg/kg TID-QID, PO-available in Lomotil</p>
<p><strong>5-HT3 Serotonin Antagonists</strong> &#8211; Antagonists of the neuronal 5-HT3 receptor    inhibit Cl- and H2O secretion from intestinal epithelial cells.</p>
<p>1. Ondansetron (Zofran, Glaxo) &#8211; 0.5-1.0 mg/kg BID, PO</p>
<p>2. Granisetron (Kytril, SmithKline Beecham) &#8211; 0.5-1.0 mg/kg BID, PO</p>
<p><strong>Adrenergic Antagonists</strong> &#8211; These drugs must be used carefully as they    can activate -adrenergic receptors in the chemoreceptor trigger zone and cause    vomiting.</p>
<p>1. Clonidine 5-10 ?/kg BID-TID, SQ/PO</p>
<p><strong>Restoration of G.I. Motility</strong></p>
<p>The mixed m,d-opioid agonist, loperamide, stimulates colonic fluid and electrolyte    absorption while inhibiting colonic propulsive motility. Loperamide (0.08 mg/kg    PO TID-QID) may be beneficial in the treatment of difficult or refractory cases    of large bowel-type IBD.</p>
<p><strong>Immunosuppressive Therapy</strong></p>
<p>Sulfasalazine – Sulfasalazine is a highly effective prostaglandin synthetase    inhibitor that has proven efficacy in the therapy of large bowel IBD in the    dog. Sulfasalazine is a compound molecule of 5-aminosalicylate (meselamine)    and sulfapyridine linked in an azo chemical bond. Following oral dosing, most    of the sulfasalazine is transported to the distal gastrointestinal tract where    cecal and colonic bacteria metabolize the drug to its component parts. Sulfapyridine    is largely absorbed by the colonic mucosa but much of the 5-aminosalicylate    remains in the colonic lumen where it inhibits mucosal lipoxygenase and the    inflammatory cascade. Sulfasalazine has been recommended for the treatment of    canine large bowel IBD at doses of 10-25 mg/kg PO TID for 4-6 weeks. With resolution    of clinical signs, sulfasalazine dosages are gradually decreased by 25 per cent    at 2-week intervals and eventually discontinued while maintaining dietary management.    Salicylates are readily absorbed and induce toxicity in cats, therefore this    drug classification should be used with great caution in cats. If used in cats,    some authors have recommended using half of the recommended dog dose (i.e.,    5-12.5 mg/kg PO TID. Sulfasalazine usage has been associated with the development    of keratoconjunctivitis sicca in the dog, so tear production should be assessed    subjectively (by the pet owner) and objectively (by the veterinarian) during    usage.</p>
<p>Other 5-Aminosalicylates – This drug classification was developed to reduce    the toxicity of the sulfapyridine portion of the parent molecule (sulfasalazine)    and to enhance the efficacy of the 5-aminosalicylate portion. Meselamine (Dipentum,    Asachol) and dimeselamine (Olsalazine) are available for use in the treatment    of canine large bowel IBD. Olsalazine has been used at a dosage of 5-10 mg/kg    PO TID in the dog. Despite the formulation of sulfa-free 5-aminosalicylate preparations,    instances of keratoconjunctivitis sicca have still been reported in the dog.</p>
<p>Metronidazole – Metronidazole (10-20 mg/kg PO BID-TID) has been used in    the treatment of mild to moderate cases of large bowel IBD in both dogs and    cats. Metronidazole has been used either as a single agent or in conjunction    with 5-aminosalicylates or glucocorticoids. Metronidazole is believed to have    several beneficial properties, including anti-bacterial, anti-protozoal, and    immunomodulatory effects. Side effects include anorexia, hypersalivation, and    vomiting at recommended doses and neurotoxicity (ataxia, nystagmus, head title,    and seizures) at higher doses. Side effects usually resolve with discontinuation    of therapy but diazepam may accelerate recovery of individual patients.</p>
<p>Glucocorticoids – Anti-inflammatory doses of prednisone or prednisolone    (1-2 mg/kg PO SID) may be used to treat IBD in dogs that have failed to respond    to dietary management, sulfasalazine, or metronidazole, and as adjunctive therapy    to dietary modification in feline IBD. Prednisone or prednisolone is used most    frequently, as both have short durations of action, are cost-effective, and    are widely available. Equipotent doses of dexamethasone are equally effective    but may have more deleterious effects on brush border enzyme activity. Prednisone    should be used for 2-4 weeks depending upon the severity of the clinical signs.    Higher doses of prednisone (e.g., 2-4 mg/kg PO SID) may be needed to control    severe forms of eosinophilic colitis or hypereosinophilic syndrome in cats.    Combination therapy with sulfasalazine, metronidazole, or azothioprine may reduce    the overall dosage of prednisone needed to achieve remission of clinical signs.    As with sulfasalazine, the dose of glucocorticoid may be reduced by 25% at 1-2    week intervals while hopefully maintaining remission with dietary modification.</p>
<p>Because of steroid side effects and suppression of the hypothalamic-pituitary-adrenal    axis, several alternative glucocorticoids have been developed that have excellent    topical (i.e., mucosal) anti-inflammatory activity but are significantly metabolized    during first pass hepatic metabolism. Budesonide has been used for many years    as an inhaled medication for asthma, and an enteric-coated form of the drug    is now available for treatment of IBD in humans (and animals). There is little    evidence-based medicine in support of the use of this medication in canine or    feline IBD, but doses of 1 mg/cat or 1 mg/dog per day have been used with some    success in anecdotal cases.</p>
<p>Azathioprine – Azathioprine is a purine analog that, following DNA incorporation,    inhibits lymphocyte activation and proliferation. It is rarely effective as    a single agent, and it should instead be used as adjunctive therapy with glucocorticoids.    Azathioprine may have a significant steroid-sparing effect in IBD. Doses of    2 mg/kg PO q 24 hours in dogs and 0.3 mg/kg PO q 48 hours in cats have been    used with some success in IBD. It may take several weeks or months of therapy    for azathioprine to become maximally effective. Cats particularly should be    monitored for side effects, including myelosuppression, hepatic disease, and    acute pancreatic necrosis.</p>
<p>Cyclosporine – Cyclosporine has been used in the renal transplantation    patient for its inhibitory effect on T cell function. In more recent times,    cyclosporine has been used in a number of immune-mediated disorders, including    keratoconjunctivitis sicca, perianal fistula (anal furunculosis), and IMHA.    Anecdotal reports suggest that cyclosporine (3-7 mg/kg PO BID) may be useful    in the treatment of some cases of refractory IBD. Evidence-based medicine studies    will be needed to establish efficacy, but anecdotal experience would suggest    that cyclosporine may be useful in some of the more difficult or refractory    cases of IBD.</p>
<p>Chlorambucil – Chlorambucil (2 mg/m2 PO every other day) has been used    in place of azathioprine in some difficult or refractory cases of feline IBD.<br />
<strong>Behavioral Modification</strong></p>
<p>Inflammatory bowel disease and irritable bowel syndrome very likely have underlying    behavioral components. Abnormal personality traits and potential environmental    stress factors were identified in 38% of dogs in one study. Multiple factors    were present in affected households, including travel, re-location, house construction,    separation anxiety, submissive urination, noise sensitivity, and aggression.    The role of behavior in the pathogenesis and therapy of canine and feline gastrointestinal    disorders remains largely unexplored.</p>
<p>References – Available upon request.</p>
<p>Minnesota Veterinary Medical Association Gastroenterology</p>
<p><a href="http://www.mvma.org/Proceedings/Small%20Animal%20Gastro/GastroenterologyTOC.html">http://www.mvma.org/Proceedings/Small%20Animal%20Gastro/GastroenterologyTOC.html</a></p>
<p><a href="http://www.mvma.org/Proceedings/Small%20Animal%20Gastro/Canine%20IBD.html">http://www.mvma.org/Proceedings/Small%20Animal%20Gastro/Canine%20IBD.html</a></p>
<p>Robert J. Washabau, VMD, PhD, Dipl. ACVIM<br />
Professor of Medicine and Department Chair<br />
Department of Veterinary Clinical Sciences<br />
College of Veterinary Medicine, University of Minnesota<br />
St. Paul, Minnesota 55108 U.S.A.<br />
(612) 625-5273 Office; (612) 624-0751 FAX<br />
E-Mail:washabau@umn.edu<</p>
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		<title>Breed related risks for bloat</title>
		<link>http://webcanine.com/2007/breed-related-risks-for-bloat/</link>
		<comments>http://webcanine.com/2007/breed-related-risks-for-bloat/#comments</comments>
		<pubDate>Wed, 25 Apr 2007 01:31:55 +0000</pubDate>
		<dc:creator>mom</dc:creator>
				<category><![CDATA[Bloat (GDV)]]></category>
		<category><![CDATA[Diet and Feeding]]></category>
		<category><![CDATA[bloat]]></category>
		<category><![CDATA[gdv]]></category>

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		<description><![CDATA[<p align="center">GRANT</p>
<p align="center"> Incidence and Breed Related Risk Factors for Gastric Dilation-Volvulus                in Dogs
5-year prospective study by Larry Glickman, VMD, Ph.D., Purdue University</p>
<p>Participating breed clubs Akita, Bloodhound, Collie, Great Dane,            <span style="color:#777"> . . . &#8594; Read More: <a href="http://webcanine.com/2007/breed-related-risks-for-bloat/">Breed related risks for bloat</a></span>]]></description>
			<content:encoded><![CDATA[<p align="center">GRANT</p>
<p align="center"> <strong>Incidence and Breed Related Risk Factors for Gastric Dilation-Volvulus                in Dogs<br />
5-year prospective study by Larry Glickman, VMD, Ph.D., Purdue University</strong></p>
<p>Participating breed clubs Akita, Bloodhound, Collie, Great Dane,                Irish Setter, Irish Wolfhound, Newfoundland, Rottweiler, Saint Bernard,                Standard Poodle, Weimaraner and the AKC/CHF.<br />
<strong>Method</strong></p>
<p>Investigator measured dogs at dog shows and the owners completed                a detailed questionnaire concerning the dogs medical history, genetic                background, husbandry and eating practices, personality and diet.</p>
<p>Five years later, the investigator called and conducted a follow-up                on each the dog.<br />
The incidence of bloat (GDV) was calculated for each breed.<br />
Risk factors were compared to dog measurements and questionnaire                responses to determine any correlation.   Results: <span id="more-20"></span><br />
<strong>STUDY COMPLETED</strong><br />
Results for the Rottweiler<br />
(Data based on 200 dogs)</p>
<p>* Of the 11 breeds tested, the Rottweiler had the lowest incidence                of Bloat (1%).<br />
* &#8220;Happy/easy going&#8221; dogs were found to be less prone                to bloat. Rottweiler was listed as the easiest going/confident dog                of the 11 breeds surveyed.<br />
* Overweight dogs were less prone to bloat.<br />
* Dogs that are feed 2 &#8211; 3 times a day are less prone to bloat.<br />
* <strong>Restricting water before or after eating, or elevating the dogs                food bowl increased the incidence of bloat.</strong><br />
* Bloat incidence was found to increase with age.<br />
*<em> Giving dogs anti-gas medication on a <strong>regular basis</strong>,                increased the incidence of bloat by 66%.</em><br />
* Do not breed any animal if there has been a  relative that has                previously bloated.</p>
<p><a href="http://www.rottweilerhealth.org/grants_funded.html">http://www.rottweilerhealth.org/grants_funded.html<</p>
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		<title>Gastropexy</title>
		<link>http://webcanine.com/2007/gastropexy/</link>
		<comments>http://webcanine.com/2007/gastropexy/#comments</comments>
		<pubDate>Wed, 25 Apr 2007 01:29:35 +0000</pubDate>
		<dc:creator>mom</dc:creator>
				<category><![CDATA[Bloat (GDV)]]></category>
		<category><![CDATA[Diet and Feeding]]></category>
		<category><![CDATA[bloat]]></category>
		<category><![CDATA[gdv]]></category>

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		<description><![CDATA[<p>Gastropexy</p>
<p>Finding on use of  gastropexy for                dog owners:</p>
<p>In a study of 1,920 dogs at risk the following recommendations                can be made regarding prophylaxis for bloat:</p>
<p>1 <span style="color:#777"> . . . &#8594; Read More: <a href="http://webcanine.com/2007/gastropexy/">Gastropexy</a></span>]]></description>
			<content:encoded><![CDATA[<p><span style="font-size: medium;"><strong>Gastropexy</strong></span></p>
<p><span style="color: #0000ff;"><em><a href="http://www.vet.purdue.edu/epi/pups.htm"></a></em><span style="color: #000000;">Finding on use of <em> <strong>gastropexy</strong></em> </span><span style="color: #000000;">for                dog owners:</span></span></p>
<p>In a study of 1,920 dogs at risk the following recommendations                can be made regarding prophylaxis for bloat:</p>
<p>1 &#8211; with prophylactic gastropexy; after an episode of bloat, gastropexy                decreased GDV recurrence by 95%. We would consider it to be just                as effective as a preventive measure on dogs at risk for GDV (ie;                all deep- chested dogs, dogs with first degree relatives with GDV)                You should go to a veterinary surgeon to perform the surgery                as many vets do this procedure regularly. Also these dogs                should be sterilized to prevent passing on bloat risk to their progeny.</p>
<p>2 -Add Simethicone to each feeding (adult human dose)</p>
<p>I believe          if the risk of GDV developing in a dog&#8217;s lifetime  is high, then it is          appropriate for owners and veterinarians to  consider performing a prophylactic          gastropexy (a surgical  procedure to prevent the stomach from rotating)          in order to  prevent a first episode of GDV from occurring. However, I would not recommend  that prophylactic gastropexy be done          unless the dog were  surgically neutered, so as not to increase the pool          of dogs in a  breed that are prone to develop GDV. Persons considering           prophylactic gastropexy for their dog should discuss the procedure with           their veterinarian and with owners of dogs that have had this  procedure.</p>
<p><strong> </strong></p>
<p>To find a veterinarian in your state who performs this surgery I would search for : <strong>Board Certified Veterinary Surgeon</strong> (<em>your state</em>).  Unfortunately, the American College of Veterinary Surgeons does not at  this time have a complete listing of Certified surgeons by state.</p>
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		<title>Diet related risks for bloat</title>
		<link>http://webcanine.com/2007/diet-related-risks-for-bloat/</link>
		<comments>http://webcanine.com/2007/diet-related-risks-for-bloat/#comments</comments>
		<pubDate>Wed, 25 Apr 2007 01:27:02 +0000</pubDate>
		<dc:creator>mom</dc:creator>
				<category><![CDATA[Bloat (GDV)]]></category>
		<category><![CDATA[Diet and Feeding]]></category>
		<category><![CDATA[bloat]]></category>
		<category><![CDATA[diet and bloat]]></category>
		<category><![CDATA[gdv]]></category>

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		<description><![CDATA[<p>GDV (Bloat) and diet
</p>
<p> Summary: Dogs at risk for bloat (deep chested                dogs) should not be fed on raised food bowls, or a food that                has <span style="color:#777"> . . . &#8594; Read More: <a href="http://webcanine.com/2007/diet-related-risks-for-bloat/">Diet related risks for bloat</a></span>]]></description>
			<content:encoded><![CDATA[<p><strong><span style="font-size: medium;">GDV (Bloat) and diet<br />
</span></strong></p>
<p><strong> Summary:</strong> Dogs at risk for bloat (deep chested                dogs) should <em>not</em> be fed on raised food bowls, or a food that                has FAT as one of the 1st four ingredients, or fed foods with citric                acid that are moistened. They <em>should</em> be fed food that has                a rendered meat with bone in the first four ingredients. We  recommend that you evaluate the food choices by reviewing several sources such as ; <a href="http://docs.google.com/viewer?a=v&amp;q=cache:JvRlx3DGrKMJ:dels-old.nas.edu/banr/briefs/dog_nutrition_final.pdf+National+Research+Council+animal+nutrition+series+dog+nutrition&amp;hl=en&amp;gl=us&amp;pid=bl&amp;srcid=ADGEESj6_9xE9DG8k2Mm09qDKArNtzMqmnM5qTLBKi1LHfloR5VtaIXgxT8vLyXBJzI4_NXDWZfvq9J0rK9QWncoQWTyZ4YW44FirlLKVeJhxP88bUakswJLr2hn3r2xNCkJ5oJtPyJh&amp;sig=AHIEtbRAvc8LfVC4IVP-a-VKVopVhq3L2Q" target="_blank">Your dog&#8217;s nutritional needs.,<br />
<em></em></a><em><a href="http://www.dogfoodanalysis.com/dog-food-index-a.html" target="_blank">http://www.dogfoodanalysis.com/dog-food-index-a.html<br />
</a></em><a href="http://www.epettalk.com/forums/content.php?28-2010-Whole-Dog-%20Journal-s-Recommended-DRY-Food-List" target="_blank">WDJ dog food recommendations.</a><a href="http://docs.google.com/viewer?a=v&amp;q=cache:JvRlx3DGrKMJ:dels-old.nas.edu/banr/briefs/dog_nutrition_final.pdf+National+Research+Council+animal+nutrition+series+dog+nutrition&amp;hl=en&amp;gl=us&amp;pid=bl&amp;srcid=ADGEESj6_9xE9DG8k2Mm09qDKArNtzMqmnM5qTLBKi1LHfloR5VtaIXgxT8vLyXBJzI4_NXDWZfvq9J0rK9QWncoQWTyZ4YW44FirlLKVeJhxP88bUakswJLr2hn3r2xNCkJ5oJtPyJh&amp;sig=AHIEtbRAvc8LfVC4IVP-a-VKVopVhq3L2Q" target="_blank"></a><a href="http://www.dogfoodanalysis.com/dog-food-index-a.html" target="_blank"></a></p>
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<p><strong>Dietary Risk Factors for Gastric Dilatation-Volvulus (Bloat)                in 11 Large and Giant Dog Breeds: A Nested Case-Control Study </strong></p>
<p>ABSTRACT *Malathi Raghavan, DVM, MS; Lawrence T. Glickman, VMD,                DrPH; Nita W. Glickman, MS, MPH; Diana B. Schellenberg, MS.</p>
<p>Dietary risk factors for gastric dilatation-volvulus (GDV) in dogs                were identified using a nested case-control study. Of 1,991 dogs                from 11 large- and giant-breeds in a previous prospective study                of GDV, 106 dogs that developed GDV were selected as cases while                212 remaining dogs were randomly selected as controls. A complete                profile of nutrient intake was constructed for each dog based on                owner-reported information, published references and nutrient databases.                Potential risk factors were examined for a significant (p&lt;0.05)                relationship with GDV risk using unconditional logistic regression.</p>
<p><strong>The study confirmed previous reports of increased risks of                GDV associated with increasing age, having a first-degree relative                with GDV, and having a raised food bowl. New significant findings                included a 2.7-fold (or 170%) increased risk of GDV in dogs that                consumed dry foods containing fat among the first four ingredients.</strong> <strong>The risk of GDV was increased 4.2-fold (or 320%) in dogs that                consumed dry foods containing citric acid that were also moistened                prior to feeding by owners. Dry foods containing a rendered meat                meal with bone among the first four ingredients significantly decreased                GDV risk by 53.0%. Approximately 30% of all cases of GDV in this                study could be attributed to consumption of dry foods containing                fat among their first four ingredients, while 32% could be attributed                to consumption of owner-moistened dry foods that also contained                citric acid. These findings can be used by owners to reduce their                dogs&#8217; risk of GDV.</strong></p>
<p>This manuscript has been accepted for publication in the / Journal                of the Animal Hospital Association /(JAAHA).</p>
<p>Tufts University: Risk Factors for Canine bloat from Canine and Feline Breeding                and Genetics Conference 2003 <a href="http://www.vin.com/proceedings/Proceedings.plx?CID=TUFTSBG2003&amp;PID=5091&amp;O=Generic">http://www.vin.com/proceedings/Proceedings.plx?CID=TUFTSBG2003&amp;PID=5091&amp;O=Generic</a><br />
<a href="http://www.webcanine.com/medsurgbloat.htm"></a></p>
<p><a href="http://webcanine.com/2007/med-surg-treatment-for-bloat/#more-107" target="_blank">Medical Surgical treatment for bloat.</a></p>
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