<?xml version="1.0" encoding="UTF-8"?>
<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#"><channel rdf:about="http://onlinelibrary.wiley.com/rss/journal/10.1111/(ISSN)1476-4431" xmlns="http://purl.org/rss/1.0/"><title>Journal of Veterinary Emergency and Critical Care</title><description> Wiley Online Library : Journal of Veterinary Emergency and Critical Care</description><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2F%28ISSN%291476-4431</link><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc</dc:publisher><dc:language xmlns:dc="http://purl.org/dc/elements/1.1/">en</dc:language><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/">© Veterinary Emergency and Critical Care Society</dc:rights><prism:issn xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">1479-3261</prism:issn><prism:eIssn xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">1476-4431</prism:eIssn><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-01T00:00:00-05:00</dc:date><prism:coverDisplayDate xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">March/April 2013</prism:coverDisplayDate><prism:volume xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">23</prism:volume><prism:number xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">2</prism:number><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">111</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">262</prism:endingPage><image rdf:resource="http://onlinelibrary.wiley.com/store/10.1111/(ISSN)1476-4431/asset/cover.gif?v=1&amp;s=c66abfccfe9ed26e03ecbdb390d036bf6478a1db"/><items><rdf:Seq><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12053"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12049"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12056"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12055"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12054"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12052"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12051"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12050"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12048"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12047"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12038"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12037"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12029"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12014"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12039"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12030"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12032"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12036"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12026"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12027"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12031"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12028"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12034"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12033"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12035"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12040"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12041"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12042"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12043"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12044"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12045"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12046"/></rdf:Seq></items></channel><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12053" xmlns="http://purl.org/rss/1.0/"><title>The use of high-dose insulin therapy and intravenous lipid emulsion to treat severe, refractory diltiazem toxicosis in a dog</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12053</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">The use of high-dose insulin therapy and intravenous lipid emulsion to treat severe, refractory diltiazem toxicosis in a dog</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Barbara L. Maton, Erin E. Simmonds, Justine A. Lee, Amy J. Alwood</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-05-08T11:53:24.730872-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/vec.12053</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/vec.12053</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12053</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Case Report</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="vec12053-sec-0010" xmlns="http://www.w3.org/1999/xhtml"><h4>Objective</h4><div class="para"><p>To describe the novel use of high-dose insulin (HDI) therapy and intravenous lipid emulsion (ILE) to treat refractory, severe diltiazem toxicosis in a dog.</p></div></div>
<div class="section" id="vec12053-sec-0020" xmlns="http://www.w3.org/1999/xhtml"><h4>Case Summary</h4><div class="para"><p>A 4-year-old Pomeranian was presented for treatment 2.5 hours following ingestion of a diltiazem extended-release capsule. Toxic ingestion was calculated at a maximum exposure of 79 mg/kg, with a reported canine LD<sub>50</sub> of 50 mg/kg. Clinical signs of progressive hypotension and severe bradycardia with atrial standstill were observed, which persisted despite treatment with atropine, calcium, glucagon, and dopamine. The novel use of HDI and ILE as part of therapy for diltiazem toxicosis resulted in clinical resolution of life-threatening signs. Within 1 hour of initiating HDI therapy, the clinical signs improved, and with continued treatment, the patient remained normotensive and survived to discharge.</p></div></div>
<div class="section" id="vec12053-sec-0030" xmlns="http://www.w3.org/1999/xhtml"><h4>New or Unique Information Provided</h4><div class="para"><p>To the authors’ knowledge, this is the first reported clinical case describing the use of both HDI and ILE therapy in the treatment of severe refractory diltiazem toxicosis in veterinary medicine. No significant adverse effects were observed from the treatment. In veterinary patients with severe refractory calcium channel blocker toxicosis, the use of HDI and ILE should be considered for life-threatening clinical signs.</p></div></div>
]]></content:encoded><description>


Objective
To describe the novel use of high-dose insulin (HDI) therapy and intravenous lipid emulsion (ILE) to treat refractory, severe diltiazem toxicosis in a dog.


Case Summary
A 4-year-old Pomeranian was presented for treatment 2.5 hours following ingestion of a diltiazem extended-release capsule. Toxic ingestion was calculated at a maximum exposure of 79 mg/kg, with a reported canine LD50 of 50 mg/kg. Clinical signs of progressive hypotension and severe bradycardia with atrial standstill were observed, which persisted despite treatment with atropine, calcium, glucagon, and dopamine. The novel use of HDI and ILE as part of therapy for diltiazem toxicosis resulted in clinical resolution of life-threatening signs. Within 1 hour of initiating HDI therapy, the clinical signs improved, and with continued treatment, the patient remained normotensive and survived to discharge.


New or Unique Information Provided
To the authors’ knowledge, this is the first reported clinical case describing the use of both HDI and ILE therapy in the treatment of severe refractory diltiazem toxicosis in veterinary medicine. No significant adverse effects were observed from the treatment. In veterinary patients with severe refractory calcium channel blocker toxicosis, the use of HDI and ILE should be considered for life-threatening clinical signs.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12049" xmlns="http://purl.org/rss/1.0/"><title>Use of viscoelastic coagulation testing to monitor low molecular weight heparin administration to healthy horses</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12049</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Use of viscoelastic coagulation testing to monitor low molecular weight heparin administration to healthy horses</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Brett S. Tennent-Brown, Kira L. Epstein, Dorothy D. Whelchel, Steeve Giguère</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-05-08T11:53:14.741262-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/vec.12049</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/vec.12049</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12049</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Original Study</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="vec12049-sec-0010" xmlns="http://www.w3.org/1999/xhtml"><h4>Objectives</h4><div class="para"><p>To evaluate the utility of thromboelastography (TEG) and Sonoclot analyses to monitor the effects of low molecular weight heparin (LMWH) administration to healthy horses.</p></div></div>
<div class="section" id="vec12049-sec-0020" xmlns="http://www.w3.org/1999/xhtml"><h4>Design</h4><div class="para"><p>Randomized crossover study.</p></div></div>
<div class="section" id="vec12049-sec-0030" xmlns="http://www.w3.org/1999/xhtml"><h4>Setting</h4><div class="para"><p>Large animal veterinary teaching hospital.</p></div></div>
<div class="section" id="vec12049-sec-0040" xmlns="http://www.w3.org/1999/xhtml"><h4>Animals</h4><div class="para"><p>Six adult mixed breed healthy mares.</p></div></div>
<div class="section" id="vec12049-sec-0050" xmlns="http://www.w3.org/1999/xhtml"><h4>Interventions</h4><div class="para"><p>LMWH (dalteparin) was administered (50 U/kg subcutaneously) either every 12 or 24 h for 3 consecutive days. Blood samples were collected before LMWH administration and then at selected time points for analysis. Thromboelastography derived R-time (R), K-time (K), angle (ANG), and maximum amplitude (MA), and Sonoclot activated clot time (ACT), clot rate (CR), and platelet function (PF) were measured in whole blood 30 min after sample collection. Change (Δ) and percentage change (%Δ) from baseline of each TEG and Sonoclot variable were subsequently calculated. Anti-factor Xa activity and activated partial thromboplastin time (aPTT) were assayed in harvested plasma. The association between anti-factor Xa activity and TEG and Sonoclot (measured and calculated) variables was assessed by calculating correlation coefficients and multiple regression analysis. The ability of measured and calculated TEG and Sonoclot variables to predict when anti-factor Xa activity fell below suggested thromboprophylactic levels was assessed using receiver operating characteristic curve analysis.</p></div></div>
<div class="section" id="vec12049-sec-0060" xmlns="http://www.w3.org/1999/xhtml"><h4>Measurements and Main Results</h4><div class="para"><p>The correlation between aPTT and anti-factor Xa activity was weak (<em>r</em> = 0.343). Changes in TEG and Sonoclot variables following LMWH administration were consistent with hypocoagulation. All measured and calculated TEG variables were significantly correlated with anti-factor Xa activity. Sonoclot ACT, ΔACT, CR, ΔCR, and %ΔCR were also significantly correlated with anti-factor Xa activity. TEG ΔR and %ΔR best predicted anti-factor Xa activity below the suggested thromboprophylactic level.</p></div></div>
<div class="section" id="vec12049-sec-0070" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Although correlations were modest, serial measurement of TEG variables may be used to monitor LMWH therapy in horses; however, further research is required in sick horses.</p></div></div>
]]></content:encoded><description>


Objectives
To evaluate the utility of thromboelastography (TEG) and Sonoclot analyses to monitor the effects of low molecular weight heparin (LMWH) administration to healthy horses.


Design
Randomized crossover study.


Setting
Large animal veterinary teaching hospital.


Animals
Six adult mixed breed healthy mares.


Interventions
LMWH (dalteparin) was administered (50 U/kg subcutaneously) either every 12 or 24 h for 3 consecutive days. Blood samples were collected before LMWH administration and then at selected time points for analysis. Thromboelastography derived R-time (R), K-time (K), angle (ANG), and maximum amplitude (MA), and Sonoclot activated clot time (ACT), clot rate (CR), and platelet function (PF) were measured in whole blood 30 min after sample collection. Change (Δ) and percentage change (%Δ) from baseline of each TEG and Sonoclot variable were subsequently calculated. Anti-factor Xa activity and activated partial thromboplastin time (aPTT) were assayed in harvested plasma. The association between anti-factor Xa activity and TEG and Sonoclot (measured and calculated) variables was assessed by calculating correlation coefficients and multiple regression analysis. The ability of measured and calculated TEG and Sonoclot variables to predict when anti-factor Xa activity fell below suggested thromboprophylactic levels was assessed using receiver operating characteristic curve analysis.


Measurements and Main Results
The correlation between aPTT and anti-factor Xa activity was weak (r = 0.343). Changes in TEG and Sonoclot variables following LMWH administration were consistent with hypocoagulation. All measured and calculated TEG variables were significantly correlated with anti-factor Xa activity. Sonoclot ACT, ΔACT, CR, ΔCR, and %ΔCR were also significantly correlated with anti-factor Xa activity. TEG ΔR and %ΔR best predicted anti-factor Xa activity below the suggested thromboprophylactic level.


Conclusions
Although correlations were modest, serial measurement of TEG variables may be used to monitor LMWH therapy in horses; however, further research is required in sick horses.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12056" xmlns="http://purl.org/rss/1.0/"><title>Evaluation of a training course in focused echocardiography for noncardiology house officers</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12056</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Evaluation of a training course in focused echocardiography for noncardiology house officers</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Yuki C. Tse, John E. Rush, Suzanne M. Cunningham, Barret J. Bulmer, Lisa M. Freeman, Elizabeth A. Rozanski</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-05-06T10:02:38.631838-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/vec.12056</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/vec.12056</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12056</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Original Study</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="vec12056-sec-0010" xmlns="http://www.w3.org/1999/xhtml"><h4>Objective</h4><div class="para"><p>To determine whether a training course in focused echocardiography can improve the proficiency of noncardiology house officers in accurately interpreting cardiovascular disease and echocardiography findings in dogs entering the emergency room setting.</p></div></div>
<div class="section" id="vec12056-sec-0020" xmlns="http://www.w3.org/1999/xhtml"><h4>Design</h4><div class="para"><p>Prospective, blinded, educational study.</p></div></div>
<div class="section" id="vec12056-sec-0030" xmlns="http://www.w3.org/1999/xhtml"><h4>Setting</h4><div class="para"><p>University veterinary teaching hospital.</p></div></div>
<div class="section" id="vec12056-sec-0040" xmlns="http://www.w3.org/1999/xhtml"><h4>Study Subjects</h4><div class="para"><p>House officers underwent training in focused echocardiography. Fifteen dogs, including normal dogs and dogs with stable congenital or acquired cardiac disease, were used as study subjects during the laboratory session.</p></div></div>
<div class="section" id="vec12056-sec-0050" xmlns="http://www.w3.org/1999/xhtml"><h4>Interventions</h4><div class="para"><p>A 6-hour curriculum on focused echocardiography was developed that included didactic lectures, clinical cases, and hands-on echocardiography.</p></div></div>
<div class="section" id="vec12056-sec-0060" xmlns="http://www.w3.org/1999/xhtml"><h4>Measurements and Main Results</h4><div class="para"><p>Pre- and postcourse written examinations were administered to participants. House officers attended didactic lectures that were subsequently followed by a hands-on laboratory session and practical examination, which involved performing transthoracic echocardiography on dogs with and without cardiovascular disease. Twenty-one house officers completed the focused echocardiography training course. Written examination scores were 57 ± 12% before and 75 ± 10% after training (<em>P</em> &lt; 0.001). Following the course, 97% of participants in the practical examination were able to obtain the correct right parasternal short- or long-axis view. Posttraining, most participants correctly identified pleural effusion (90%) and pericardial effusion (95%) and discriminated normal atrial size from atrial enlargement (86%). However, successful identification of a cardiac mass, volume status, and ability to recognize a poor quality study as nondiagnostic remained relatively low. Most trainees responded that the length of hands-on laboratory training was too abbreviated and that the course should be &gt; 6 hours.</p></div></div>
<div class="section" id="vec12056-sec-0070" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusion</h4><div class="para"><p>A focused echocardiography training course improved knowledge and yielded acceptable proficiency in some echocardiographic findings commonly identified in the emergency room. This training course was not able to provide the skills needed for house officers to accurately assess fluid volume status, identify cardiac masses, ventricular enlargement or hypertrophy, and certain cardiac diseases.</p></div></div>
]]></content:encoded><description>


Objective
To determine whether a training course in focused echocardiography can improve the proficiency of noncardiology house officers in accurately interpreting cardiovascular disease and echocardiography findings in dogs entering the emergency room setting.


Design
Prospective, blinded, educational study.


Setting
University veterinary teaching hospital.


Study Subjects
House officers underwent training in focused echocardiography. Fifteen dogs, including normal dogs and dogs with stable congenital or acquired cardiac disease, were used as study subjects during the laboratory session.


Interventions
A 6-hour curriculum on focused echocardiography was developed that included didactic lectures, clinical cases, and hands-on echocardiography.


Measurements and Main Results
Pre- and postcourse written examinations were administered to participants. House officers attended didactic lectures that were subsequently followed by a hands-on laboratory session and practical examination, which involved performing transthoracic echocardiography on dogs with and without cardiovascular disease. Twenty-one house officers completed the focused echocardiography training course. Written examination scores were 57 ± 12% before and 75 ± 10% after training (P &lt; 0.001). Following the course, 97% of participants in the practical examination were able to obtain the correct right parasternal short- or long-axis view. Posttraining, most participants correctly identified pleural effusion (90%) and pericardial effusion (95%) and discriminated normal atrial size from atrial enlargement (86%). However, successful identification of a cardiac mass, volume status, and ability to recognize a poor quality study as nondiagnostic remained relatively low. Most trainees responded that the length of hands-on laboratory training was too abbreviated and that the course should be &gt; 6 hours.


Conclusion
A focused echocardiography training course improved knowledge and yielded acceptable proficiency in some echocardiographic findings commonly identified in the emergency room. This training course was not able to provide the skills needed for house officers to accurately assess fluid volume status, identify cardiac masses, ventricular enlargement or hypertrophy, and certain cardiac diseases.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12055" xmlns="http://purl.org/rss/1.0/"><title>Preliminary evaluation of tear production in dogs hospitalized in an intensive care unit</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12055</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Preliminary evaluation of tear production in dogs hospitalized in an intensive care unit</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Jaime A. Chandler, Alexandra Woerdt, Jennifer E. Prittie, Lou Chang</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-05-06T10:02:25.162132-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/vec.12055</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/vec.12055</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12055</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Original Study</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="vec12055-sec-0010" xmlns="http://www.w3.org/1999/xhtml"><h4>Objective</h4><div class="para"><p>To determine the tear production in dogs admitted to an intensive care unit (ICU).</p></div></div>
<div class="section" id="vec12055-sec-0020" xmlns="http://www.w3.org/1999/xhtml"><h4>Design</h4><div class="para"><p>Prospective observational study from November 2010–September 2011.</p></div></div>
<div class="section" id="vec12055-sec-0030" xmlns="http://www.w3.org/1999/xhtml"><h4>Setting</h4><div class="para"><p>Private emergency and referral hospital.</p></div></div>
<div class="section" id="vec12055-sec-0040" xmlns="http://www.w3.org/1999/xhtml"><h4>Animals</h4><div class="para"><p>Thirty healthy control dogs and 30 dogs hospitalized in an ICU for treatment of systemic illness without previously diagnosed ophthalmic disorders and no recent history of anesthesia. Enrollment was based on availability of the ophthalmologist within 24 hours of admission to the ICU.</p></div></div>
<div class="section" id="vec12055-sec-0050" xmlns="http://www.w3.org/1999/xhtml"><h4>Interventions</h4><div class="para"><p>Tear production was measured utilizing Schirmer tear test strips (STT) in healthy control animals as well as in hospitalized canine patients. All patients received an ophthalmic examination by a board-certified veterinary ophthalmologist within 24 hours of admission to the ICU. Lubrication with artificial tear gel every 2–4 hours as needed was implemented after STT was measured.</p></div></div>
<div class="section" id="vec12055-sec-0060" xmlns="http://www.w3.org/1999/xhtml"><h4>Measurements and Main Results</h4><div class="para"><p>Average tear productions in the control and canine ICU populations were 24.5 mm/min and 13.2 mm/min, respectively. This was found to be statistically significant (<em>P</em> &lt; 0.001). Furthermore, there was a trend toward a decrease in tear production in patients with kidney disease and a trend toward normal tear production in patients with cardiac disease but the sample size was likely too small to enable detection of a statistically significant difference.</p></div></div>
<div class="section" id="vec12055-sec-0070" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>This study demonstrates a decrease in tear production in canine ICU patients. While further study is warranted to determine how different diseases impact tear production, these finding support the implementation of frequent ocular lubrication in all ICU patients.</p></div></div>
]]></content:encoded><description>


Objective
To determine the tear production in dogs admitted to an intensive care unit (ICU).


Design
Prospective observational study from November 2010–September 2011.


Setting
Private emergency and referral hospital.


Animals
Thirty healthy control dogs and 30 dogs hospitalized in an ICU for treatment of systemic illness without previously diagnosed ophthalmic disorders and no recent history of anesthesia. Enrollment was based on availability of the ophthalmologist within 24 hours of admission to the ICU.


Interventions
Tear production was measured utilizing Schirmer tear test strips (STT) in healthy control animals as well as in hospitalized canine patients. All patients received an ophthalmic examination by a board-certified veterinary ophthalmologist within 24 hours of admission to the ICU. Lubrication with artificial tear gel every 2–4 hours as needed was implemented after STT was measured.


Measurements and Main Results
Average tear productions in the control and canine ICU populations were 24.5 mm/min and 13.2 mm/min, respectively. This was found to be statistically significant (P &lt; 0.001). Furthermore, there was a trend toward a decrease in tear production in patients with kidney disease and a trend toward normal tear production in patients with cardiac disease but the sample size was likely too small to enable detection of a statistically significant difference.


Conclusions
This study demonstrates a decrease in tear production in canine ICU patients. While further study is warranted to determine how different diseases impact tear production, these finding support the implementation of frequent ocular lubrication in all ICU patients.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12054" xmlns="http://purl.org/rss/1.0/"><title>Successful outcome in a dog with neurological and respiratory signs following smoke inhalation</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12054</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Successful outcome in a dog with neurological and respiratory signs following smoke inhalation</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Julien Guillaumin, Kate Hopper</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-05-06T10:02:04.159853-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/vec.12054</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/vec.12054</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12054</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Case Report</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="vec12054-sec-0010" xmlns="http://www.w3.org/1999/xhtml"><h4>Objective</h4><div class="para"><p>To report the case management of a patient with smoke inhalation complicated by neurological impairment, carboxyhemoglobinemia, acute respiratory distress syndrome (ARDS), upper airway obstruction, aspiration pneumonia, and bacteremia.</p></div></div>
<div class="section" id="vec12054-sec-0020" xmlns="http://www.w3.org/1999/xhtml"><h4>Case Summary</h4><div class="para"><p>A 1.5-year-old male intact Beagle presented shortly after being involved in a household fire. Upon arrival the dog was diagnosed with ARDS and demonstrated acute neurological signs (eg, obtundation and seizures). Treatment included mechanical ventilation, temporary tracheostomy, and intensive supportive care. During hospitalization, the dog suffered multiple complications including prolonged neurological abnormalities, aspiration pneumonia, and bacteremia. The dog recovered over a 16-day period.</p></div></div>
<div class="section" id="vec12054-sec-0030" xmlns="http://www.w3.org/1999/xhtml"><h4>New or Unique Information Provided</h4><div class="para"><p>This is the first description of extensive management of a patient suffering both neurological and respiratory complication due to smoke inhalation, and details the steps that were taken to achieve a successful outcome.</p></div></div>
]]></content:encoded><description>


Objective
To report the case management of a patient with smoke inhalation complicated by neurological impairment, carboxyhemoglobinemia, acute respiratory distress syndrome (ARDS), upper airway obstruction, aspiration pneumonia, and bacteremia.


Case Summary
A 1.5-year-old male intact Beagle presented shortly after being involved in a household fire. Upon arrival the dog was diagnosed with ARDS and demonstrated acute neurological signs (eg, obtundation and seizures). Treatment included mechanical ventilation, temporary tracheostomy, and intensive supportive care. During hospitalization, the dog suffered multiple complications including prolonged neurological abnormalities, aspiration pneumonia, and bacteremia. The dog recovered over a 16-day period.


New or Unique Information Provided
This is the first description of extensive management of a patient suffering both neurological and respiratory complication due to smoke inhalation, and details the steps that were taken to achieve a successful outcome.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12052" xmlns="http://purl.org/rss/1.0/"><title>Comparison of a gel column blood typing method and a point-of-care cartridge for Dog Erythrocyte Antigen 1.1</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12052</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Comparison of a gel column blood typing method and a point-of-care cartridge for Dog Erythrocyte Antigen 1.1</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Shauna L. Blois, Danielle M. Richardson, Anthony C. G. Abrams-Ogg</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-05-06T10:01:53.269128-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/vec.12052</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/vec.12052</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12052</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Brief Clinical Communication</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="vec12052-sec-0010" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Blood typing for the presence of Dog Erythrocyte Antigen (DEA) 1.1 is recommended in all donor and recipient dogs prior to transfusion of blood products. The objective of this study was to determine if a point-of-care DEA 1.1 blood typing cartridge could be used in place of the gel column typing method.</p></div></div>
<div class="section" id="vec12052-sec-0020" xmlns="http://www.w3.org/1999/xhtml"><h4>Study Design</h4><div class="para"><p>Detection of DEA 1.1 was performed using a laboratory-based gel column method and a point-of-care cartridge. A convenience sample of 30 healthy blood donors, 13 dogs with immune-mediated hemolytic anemia (IMHA) (3 of which had concurrent immune-mediated thrombocytopenia [IMT]), and 44 dogs with other diseases was included in the study.</p></div></div>
<div class="section" id="vec12052-sec-0030" xmlns="http://www.w3.org/1999/xhtml"><h4>Key Findings</h4><div class="para"><p>Agreement was observed between the tests for normal dogs and dogs with nonimmune-mediated disease in 74/74 cases. Two dogs in the IMHA group had indeterminate gel column blood typing results; 1 dog in this group had a negative gel column test result but a positive cartridge test result.</p></div></div>
<div class="section" id="vec12052-sec-0040" xmlns="http://www.w3.org/1999/xhtml"><h4>Significance</h4><div class="para"><p>There was good agreement between the 2 methods for normal dogs and dogs with nonimmune-mediated disease. Blood typing methods in dogs with IMHA should be further investigated.</p></div></div>
]]></content:encoded><description>


Background
Blood typing for the presence of Dog Erythrocyte Antigen (DEA) 1.1 is recommended in all donor and recipient dogs prior to transfusion of blood products. The objective of this study was to determine if a point-of-care DEA 1.1 blood typing cartridge could be used in place of the gel column typing method.


Study Design
Detection of DEA 1.1 was performed using a laboratory-based gel column method and a point-of-care cartridge. A convenience sample of 30 healthy blood donors, 13 dogs with immune-mediated hemolytic anemia (IMHA) (3 of which had concurrent immune-mediated thrombocytopenia [IMT]), and 44 dogs with other diseases was included in the study.


Key Findings
Agreement was observed between the tests for normal dogs and dogs with nonimmune-mediated disease in 74/74 cases. Two dogs in the IMHA group had indeterminate gel column blood typing results; 1 dog in this group had a negative gel column test result but a positive cartridge test result.


Significance
There was good agreement between the 2 methods for normal dogs and dogs with nonimmune-mediated disease. Blood typing methods in dogs with IMHA should be further investigated.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12051" xmlns="http://purl.org/rss/1.0/"><title>Retrospective analysis of clinical findings and outcome of cats with suspected rattlesnake envenomation in Southern California: 18 cases (2007–2010)</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12051</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Retrospective analysis of clinical findings and outcome of cats with suspected rattlesnake envenomation in Southern California: 18 cases (2007–2010)</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Jennifer A. Hoose, Amy Carr</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-05-06T10:01:41.090986-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/vec.12051</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/vec.12051</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12051</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Retrospective Study</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="vec12051-sec-0010" xmlns="http://www.w3.org/1999/xhtml"><h4>Objective</h4><div class="para"><p>To evaluate treatment and survival rates of cats with suspected rattlesnake envenomation.</p></div></div>
<div class="section" id="vec12051-sec-0020" xmlns="http://www.w3.org/1999/xhtml"><h4>Design</h4><div class="para"><p>Retrospective study.</p></div></div>
<div class="section" id="vec12051-sec-0030" xmlns="http://www.w3.org/1999/xhtml"><h4>Setting</h4><div class="para"><p>Veterinary emergency referral hospital in Southern California.</p></div></div>
<div class="section" id="vec12051-sec-0040" xmlns="http://www.w3.org/1999/xhtml"><h4>Animals</h4><div class="para"><p>Client-owned animals.</p></div></div>
<div class="section" id="vec12051-sec-0050" xmlns="http://www.w3.org/1999/xhtml"><h4>Interventions</h4><div class="para"><p>None.</p></div></div>
<div class="section" id="vec12051-sec-0060" xmlns="http://www.w3.org/1999/xhtml"><h4>Measurements and main results</h4><div class="para"><p>Eighteen cats were treated for suspected rattlesnake envenomation between January 2007 and August 2010. There were 3 fatalities and 15 cats survived (16% mortality rate). Two cases developed pelvic limb paresis 3–4 days post envenomation. There were no apparent adverse reactions to treatment with antivenom.</p></div></div>
<div class="section" id="vec12051-sec-0070" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Cats are presented infrequently for treatment of envenomation compared to dogs. Envenomation in cats should be treated according to guidelines established for people and dogs and administration of antivenom does not appear to be associated with adverse events. The mortality rate in this study was found to be 16%, which is higher than the mortality rate reported for dogs suspected of rattlesnake envenomation in a similar region (4.1%). Pelvic limb paresis may develop 3–4 days post envenomation but can resolve within 24 hours.</p></div></div>
]]></content:encoded><description>


Objective
To evaluate treatment and survival rates of cats with suspected rattlesnake envenomation.


Design
Retrospective study.


Setting
Veterinary emergency referral hospital in Southern California.


Animals
Client-owned animals.


Interventions
None.


Measurements and main results
Eighteen cats were treated for suspected rattlesnake envenomation between January 2007 and August 2010. There were 3 fatalities and 15 cats survived (16% mortality rate). Two cases developed pelvic limb paresis 3–4 days post envenomation. There were no apparent adverse reactions to treatment with antivenom.


Conclusions
Cats are presented infrequently for treatment of envenomation compared to dogs. Envenomation in cats should be treated according to guidelines established for people and dogs and administration of antivenom does not appear to be associated with adverse events. The mortality rate in this study was found to be 16%, which is higher than the mortality rate reported for dogs suspected of rattlesnake envenomation in a similar region (4.1%). Pelvic limb paresis may develop 3–4 days post envenomation but can resolve within 24 hours.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12050" xmlns="http://purl.org/rss/1.0/"><title>Preliminary evaluation of the utility of comparing SpO2/FiO2 and PaO2/FiO2 ratios in dogs</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12050</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Preliminary evaluation of the utility of comparing SpO2/FiO2 and PaO2/FiO2 ratios in dogs</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Janine M. Calabro, Jennifer E. Prittie, Douglas A. Palma</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-04-26T09:44:27.685131-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/vec.12050</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/vec.12050</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12050</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Original Study</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="vec12050-sec-0010" xmlns="http://www.w3.org/1999/xhtml"><h4>Objective</h4><div class="para"><p>To determine whether the ratio of pulse oximetry saturation/fraction of inspired oxygen (SpO<sub>2</sub>/FiO<sub>2</sub>, [SF]) correlates with the ratio of partial pressure of oxygen in arterial blood/FiO<sub>2</sub> (PaO<sub>2</sub>/FiO<sub>2</sub>, [PF]) in dogs.</p></div></div>
<div class="section" id="vec12050-sec-0020" xmlns="http://www.w3.org/1999/xhtml"><h4>Design</h4><div class="para"><p>Prospective, observational pilot study.</p></div></div>
<div class="section" id="vec12050-sec-0030" xmlns="http://www.w3.org/1999/xhtml"><h4>Setting</h4><div class="para"><p>Urban tertiary veterinary referral center.</p></div></div>
<div class="section" id="vec12050-sec-0040" xmlns="http://www.w3.org/1999/xhtml"><h4>Animals</h4><div class="para"><p>Thirty-eight client-owned dogs requiring assessment of oxygenation.</p></div></div>
<div class="section" id="vec12050-sec-0050" xmlns="http://www.w3.org/1999/xhtml"><h4>Interventions</h4><div class="para"><p>None.</p></div></div>
<div class="section" id="vec12050-sec-0060" xmlns="http://www.w3.org/1999/xhtml"><h4>Measurements and Main Results</h4><div class="para"><p>Arterial blood gas analysis with co-oximetry was performed on samples obtained from the dorsal pedal artery. Median SpO<sub>2</sub> was 91.5% (range 80–97%) and median PaO<sub>2</sub> was 70.1 mmHg (range 44.5–103.8 mmHg). Hypoventilation was uncommon and venous admixture was the predominant cause of hypoxemia in this population. Median SF was 435.7 (range 381.0–461.9) and median PF was 334.0 (range 211.9–494.3). Nine dogs (23.6%) had PF &lt;300; no dogs had PF below 200. SF and PF were correlated (ρ = 0.618, <em>P</em> &lt; 0.01).</p></div></div>
<div class="section" id="vec12050-sec-0070" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>SF and PF in dogs spontaneously breathing room air have good correlation, suggesting that SF may be a useful, noninvasive surrogate for PF when assessing oxygenation in canine patients. Further studies are warranted to confirm and validate this relationship in spontaneously breathing and mechanically ventilated dogs on varying levels of FiO<sub>2</sub> and to assess the ability of SF to predict outcome.</p></div></div>
]]></content:encoded><description>


Objective
To determine whether the ratio of pulse oximetry saturation/fraction of inspired oxygen (SpO2/FiO2, [SF]) correlates with the ratio of partial pressure of oxygen in arterial blood/FiO2 (PaO2/FiO2, [PF]) in dogs.


Design
Prospective, observational pilot study.


Setting
Urban tertiary veterinary referral center.


Animals
Thirty-eight client-owned dogs requiring assessment of oxygenation.


Interventions
None.


Measurements and Main Results
Arterial blood gas analysis with co-oximetry was performed on samples obtained from the dorsal pedal artery. Median SpO2 was 91.5% (range 80–97%) and median PaO2 was 70.1 mmHg (range 44.5–103.8 mmHg). Hypoventilation was uncommon and venous admixture was the predominant cause of hypoxemia in this population. Median SF was 435.7 (range 381.0–461.9) and median PF was 334.0 (range 211.9–494.3). Nine dogs (23.6%) had PF &lt;300; no dogs had PF below 200. SF and PF were correlated (ρ = 0.618, P &lt; 0.01).


Conclusions
SF and PF in dogs spontaneously breathing room air have good correlation, suggesting that SF may be a useful, noninvasive surrogate for PF when assessing oxygenation in canine patients. Further studies are warranted to confirm and validate this relationship in spontaneously breathing and mechanically ventilated dogs on varying levels of FiO2 and to assess the ability of SF to predict outcome.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12048" xmlns="http://purl.org/rss/1.0/"><title>Comparison of complication rates in dogs with nasoesophageal versus nasogastric feeding tubes</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12048</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Comparison of complication rates in dogs with nasoesophageal versus nasogastric feeding tubes</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Melissa K. Yu, Lisa M. Freeman, Cailin R. Heinze, Valerie J. Parker, Deborah E. Linder</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-04-26T09:44:22.645877-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/vec.12048</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/vec.12048</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12048</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Retrospective Study</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="vec12048-sec-0010" xmlns="http://www.w3.org/1999/xhtml"><h4>Objective</h4><div class="para"><p>To compare complication rates between nasoesophageal (NE) and nasogastric (NG) feeding tubes in dogs.</p></div></div>
<div class="section" id="vec12048-sec-0020" xmlns="http://www.w3.org/1999/xhtml"><h4>Design</h4><div class="para"><p>Retrospective study.</p></div></div>
<div class="section" id="vec12048-sec-0030" xmlns="http://www.w3.org/1999/xhtml"><h4>Setting</h4><div class="para"><p>University referral veterinary hospital.</p></div></div>
<div class="section" id="vec12048-sec-0040" xmlns="http://www.w3.org/1999/xhtml"><h4>Animals</h4><div class="para"><p>A total of 46 dogs that were fed through a NE (<em>n</em> = 28) or NG (<em>n</em> = 18) tube between January 2007 and December 2011 and that also had either thoracic radiography or computed tomography performed so that location of the distal tip of the tube in either the esophagus or stomach could be confirmed.</p></div></div>
<div class="section" id="vec12048-sec-0050" xmlns="http://www.w3.org/1999/xhtml"><h4>Interventions</h4><div class="para"><p>None.</p></div></div>
<div class="section" id="vec12048-sec-0060" xmlns="http://www.w3.org/1999/xhtml"><h4>Measurements and Main Results</h4><div class="para"><p>The medical record of each eligible case was reviewed and data recorded included signalment, underlying disease, body weight, body condition score, medications, duration of feeding, diet used, and complications observed (ie, vomiting, regurgitation, diarrhea, early tube removal, clogged tube, epistaxis, pulmonary aspiration, hyperglycemia, and refeeding syndrome). Dogs with NE tubes were significantly younger than dogs with NG tubes (<em>P</em> = 0.03) but there were no other significant differences in signalment, underlying disease, medications, duration of anorexia, percent of resting energy requirement achieved, or change in weight during tube feeding. There also was no significant difference between the NE and NG groups for any of the recorded complications. Significantly fewer dogs in the NE group died or were euthanized (3/28) compared to the NG group (7/18; <em>P</em> = 0.02) but outcome was not associated with age, underlying disease, or any of the recorded tube complications.</p></div></div>
<div class="section" id="vec12048-sec-0070" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>This study did not identify a difference in complication rate between NE and NG feeding tubes in dogs. Additional studies are required to determine the optimal terminal location of feeding tubes in dogs.</p></div></div>
]]></content:encoded><description>


Objective
To compare complication rates between nasoesophageal (NE) and nasogastric (NG) feeding tubes in dogs.


Design
Retrospective study.


Setting
University referral veterinary hospital.


Animals
A total of 46 dogs that were fed through a NE (n = 28) or NG (n = 18) tube between January 2007 and December 2011 and that also had either thoracic radiography or computed tomography performed so that location of the distal tip of the tube in either the esophagus or stomach could be confirmed.


Interventions
None.


Measurements and Main Results
The medical record of each eligible case was reviewed and data recorded included signalment, underlying disease, body weight, body condition score, medications, duration of feeding, diet used, and complications observed (ie, vomiting, regurgitation, diarrhea, early tube removal, clogged tube, epistaxis, pulmonary aspiration, hyperglycemia, and refeeding syndrome). Dogs with NE tubes were significantly younger than dogs with NG tubes (P = 0.03) but there were no other significant differences in signalment, underlying disease, medications, duration of anorexia, percent of resting energy requirement achieved, or change in weight during tube feeding. There also was no significant difference between the NE and NG groups for any of the recorded complications. Significantly fewer dogs in the NE group died or were euthanized (3/28) compared to the NG group (7/18; P = 0.02) but outcome was not associated with age, underlying disease, or any of the recorded tube complications.


Conclusions
This study did not identify a difference in complication rate between NE and NG feeding tubes in dogs. Additional studies are required to determine the optimal terminal location of feeding tubes in dogs.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12047" xmlns="http://purl.org/rss/1.0/"><title>Comparison of various solutions to dissolve critical care diet clots</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12047</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Comparison of various solutions to dissolve critical care diet clots</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Valerie J. Parker, Lisa M. Freeman</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-04-26T09:44:10.75234-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/vec.12047</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/vec.12047</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12047</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Brief Clinical Communication</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="vec12047-sec-0010" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Enteral feeding tubes are frequently placed in animals to provide assisted nutritional support; however, one major reported complication is clogging of the tubes. The goal of this study was to determine which solution is most effective at dissolving in vitro clots made using a veterinary canned critical care diet.</p></div></div>
<div class="section" id="vec12047-sec-0020" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Various solutions were tested for their ability to dissolve enteral feed clots, including water, meat tenderizers in water, predetermined amounts of pancreatic enzymes (with and without sodium bicarbonate) in water, carbonated beverages, and cranberry juice.</p></div></div>
<div class="section" id="vec12047-sec-0030" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>The solution that resulted in the greatest dissolution was ¼ teaspoon pancreatic enzymes and 325 mg sodium bicarbonate in 5 mL water, which was significantly better than all other solutions (water: <em>P</em> = 0.03; ¼ teaspoon pancreatic enzymes in water: <em>P</em> = 0.002; all others: <em>P</em> &lt; 0.001). Water was significantly better than all carbonated beverages and cranberry juice (<em>P</em> &lt; 0.001). The least successful solution was ½ teaspoon pancreatic enzymes and sodium bicarbonate in water.</p></div></div>
<div class="section" id="vec12047-sec-0040" xmlns="http://www.w3.org/1999/xhtml"><h4>Clinical Relevance</h4><div class="para"><p>Despite anecdotal reports of using carbonated beverages, cranberry juice, and ½ teaspoon pancreatic enzymes to unclog feeding tubes, all were significantly less effective than water. In vivo studies to evaluate the effectiveness of methods to unclog feeding tubes are warranted to further investigate these findings.</p></div></div>
]]></content:encoded><description>


Background
Enteral feeding tubes are frequently placed in animals to provide assisted nutritional support; however, one major reported complication is clogging of the tubes. The goal of this study was to determine which solution is most effective at dissolving in vitro clots made using a veterinary canned critical care diet.


Methods
Various solutions were tested for their ability to dissolve enteral feed clots, including water, meat tenderizers in water, predetermined amounts of pancreatic enzymes (with and without sodium bicarbonate) in water, carbonated beverages, and cranberry juice.


Results
The solution that resulted in the greatest dissolution was ¼ teaspoon pancreatic enzymes and 325 mg sodium bicarbonate in 5 mL water, which was significantly better than all other solutions (water: P = 0.03; ¼ teaspoon pancreatic enzymes in water: P = 0.002; all others: P &lt; 0.001). Water was significantly better than all carbonated beverages and cranberry juice (P &lt; 0.001). The least successful solution was ½ teaspoon pancreatic enzymes and sodium bicarbonate in water.


Clinical Relevance
Despite anecdotal reports of using carbonated beverages, cranberry juice, and ½ teaspoon pancreatic enzymes to unclog feeding tubes, all were significantly less effective than water. In vivo studies to evaluate the effectiveness of methods to unclog feeding tubes are warranted to further investigate these findings.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12038" xmlns="http://purl.org/rss/1.0/"><title>Intramuscular glargine with or without concurrent subcutaneous administration for treatment of feline diabetic ketoacidosis</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12038</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Intramuscular glargine with or without concurrent subcutaneous administration for treatment of feline diabetic ketoacidosis</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Rhett D. Marshall, Jacquie S. Rand, Marcus N. Gunew, Victor H. Menrath</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-26T12:20:34.682749-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/vec.12038</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/vec.12038</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12038</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Brief Clinical Communication</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="vec12038-sec-0010" xmlns="http://www.w3.org/1999/xhtml"><h4>Objective</h4><div class="para"><p>To describe treatment response and outcome in 15 cats with diabetic ketoacidosis (DKA) initially stabilized with glargine administered intramuscularly (IM) with or without subcutaneous (SC) glargine.</p></div></div>
<div class="section" id="vec12038-sec-0020" xmlns="http://www.w3.org/1999/xhtml"><h4>Materials and Methods</h4><div class="para"><p>Fifteen cats diagnosed with DKA were initially administered IM glargine (1–2 U) and in most cats (12/15 cats) this was combined with SC glargine (1–3 U). This was followed by intermittent IM glargine as required at intervals of 2 or more hours (range 2–22 h) and SC glargine (1–2 U) every 12 hours.</p></div></div>
<div class="section" id="vec12038-sec-0030" xmlns="http://www.w3.org/1999/xhtml"><h4>Key Findings</h4><div class="para"><p>All 15 cats survived and were discharged from hospital (median 4 d; range 2–5 d) and one-third (5/15) of cats subsequently achieved remission (median time 20 d; range 15–29 d). Complications included hypokalemia and hypophosphatemia, which were likely the result of DKA therapy rather than glargine treatment specifically.</p></div></div>
<div class="section" id="vec12038-sec-0040" xmlns="http://www.w3.org/1999/xhtml"><h4>Significance</h4><div class="para"><p>This study demonstrates that glargine administered IM is an effective treatment for DKA in cats, and may provide an alternative to regular insulin. The same vial used for initial treatment of DKA can then be used for subsequent management with SC glargine injections. Future prospective randomized controlled trials evaluating clinical outcomes in cats with DKA using different types and routes of administration of insulin are warranted. A prospective randomized controlled trial is required to compare outcomes for IM and IV administration of glargine and regular insulin in DKA cats with or without SC glargine.</p></div></div>
]]></content:encoded><description>


Objective
To describe treatment response and outcome in 15 cats with diabetic ketoacidosis (DKA) initially stabilized with glargine administered intramuscularly (IM) with or without subcutaneous (SC) glargine.


Materials and Methods
Fifteen cats diagnosed with DKA were initially administered IM glargine (1–2 U) and in most cats (12/15 cats) this was combined with SC glargine (1–3 U). This was followed by intermittent IM glargine as required at intervals of 2 or more hours (range 2–22 h) and SC glargine (1–2 U) every 12 hours.


Key Findings
All 15 cats survived and were discharged from hospital (median 4 d; range 2–5 d) and one-third (5/15) of cats subsequently achieved remission (median time 20 d; range 15–29 d). Complications included hypokalemia and hypophosphatemia, which were likely the result of DKA therapy rather than glargine treatment specifically.


Significance
This study demonstrates that glargine administered IM is an effective treatment for DKA in cats, and may provide an alternative to regular insulin. The same vial used for initial treatment of DKA can then be used for subsequent management with SC glargine injections. Future prospective randomized controlled trials evaluating clinical outcomes in cats with DKA using different types and routes of administration of insulin are warranted. A prospective randomized controlled trial is required to compare outcomes for IM and IV administration of glargine and regular insulin in DKA cats with or without SC glargine.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12037" xmlns="http://purl.org/rss/1.0/"><title>In vitro study of the effect of dog food on the adsorptive capacity of activated charcoal</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12037</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">In vitro study of the effect of dog food on the adsorptive capacity of activated charcoal</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Helen E. Wilson, Karen R. Humm</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-20T08:56:01.799425-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/vec.12037</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/vec.12037</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12037</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Original Study</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="vec12037-sec-0010" xmlns="http://www.w3.org/1999/xhtml"><h4>Objective</h4><div class="para"><p>To evaluate the effect of dog food on the adsorptive capacity of activated charcoal.</p></div></div>
<div class="section" id="vec12037-sec-0020" xmlns="http://www.w3.org/1999/xhtml"><h4>Design</h4><div class="para"><p>In vitro laboratory study.</p></div></div>
<div class="section" id="vec12037-sec-0030" xmlns="http://www.w3.org/1999/xhtml"><h4>Setting</h4><div class="para"><p>University veterinary teaching hospital.</p></div></div>
<div class="section" id="vec12037-sec-0040" xmlns="http://www.w3.org/1999/xhtml"><h4>Animals</h4><div class="para"><p>None.</p></div></div>
<div class="section" id="vec12037-sec-0050" xmlns="http://www.w3.org/1999/xhtml"><h4>Interventions</h4><div class="para"><p>None.</p></div></div>
<div class="section" id="vec12037-sec-0060" xmlns="http://www.w3.org/1999/xhtml"><h4>Materials and Methods</h4><div class="para"><p>A fixed quantity of acetaminophen (50 mg) was added to a fixed quantity of activated charcoal (1 g), mixed with varying amounts of dog food (2–14 g). The admixture was agitated for 5 minutes, incubated at 38.5°C for 1 hour and then centrifuged for 30 minutes. The concentration of residual, nonadsorbed acetaminophen in the supernatant was quantitatively assayed by reverse phase high-pressure liquid chromatography with ultraviolet detection. Data were tested by linear regression analysis and statistical significance was set at <em>P</em> &lt; 0.05.</p></div></div>
<div class="section" id="vec12037-sec-0070" xmlns="http://www.w3.org/1999/xhtml"><h4>Measurements and Main Results</h4><div class="para"><p>A statistically significant reduction in the adsorptive capacity of activated charcoal was demonstrated with increasing amounts of dog food (<em>R</em><sup>2</sup> = 0.54; <em>P</em> = 0.0018). However, all measurements of residual acetaminophen were less than 100 mg/L, representing a reduction in acetaminophen concentration of more than 98.6%.</p></div></div>
<div class="section" id="vec12037-sec-0080" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>The addition of dog food to activated charcoal reduces its total adsorptive capacity for acetaminophen. However, this reduction in adsorptive capacity is unlikely to be clinically significant in the presence of both the formulation of dog food and the ratio of dog food to charcoal used in this study.</p></div></div>
]]></content:encoded><description>


Objective
To evaluate the effect of dog food on the adsorptive capacity of activated charcoal.


Design
In vitro laboratory study.


Setting
University veterinary teaching hospital.


Animals
None.


Interventions
None.


Materials and Methods
A fixed quantity of acetaminophen (50 mg) was added to a fixed quantity of activated charcoal (1 g), mixed with varying amounts of dog food (2–14 g). The admixture was agitated for 5 minutes, incubated at 38.5°C for 1 hour and then centrifuged for 30 minutes. The concentration of residual, nonadsorbed acetaminophen in the supernatant was quantitatively assayed by reverse phase high-pressure liquid chromatography with ultraviolet detection. Data were tested by linear regression analysis and statistical significance was set at P &lt; 0.05.


Measurements and Main Results
A statistically significant reduction in the adsorptive capacity of activated charcoal was demonstrated with increasing amounts of dog food (R2 = 0.54; P = 0.0018). However, all measurements of residual acetaminophen were less than 100 mg/L, representing a reduction in acetaminophen concentration of more than 98.6%.


Conclusions
The addition of dog food to activated charcoal reduces its total adsorptive capacity for acetaminophen. However, this reduction in adsorptive capacity is unlikely to be clinically significant in the presence of both the formulation of dog food and the ratio of dog food to charcoal used in this study.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12029" xmlns="http://purl.org/rss/1.0/"><title>Clinical experience with a lipid-free, ready-made parenteral nutrition solution in dogs: 70 cases (2006–2012)</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12029</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Clinical experience with a lipid-free, ready-made parenteral nutrition solution in dogs: 70 cases (2006–2012)</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Isuru Gajanayake, Claire E. Wylie, Daniel L. Chan</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-05T10:58:51.698525-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/vec.12029</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/vec.12029</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12029</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Retrospective Study</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="vec12029-sec-0010" xmlns="http://www.w3.org/1999/xhtml"><h4>Objective</h4><div class="para"><p>To review the clinical use of a lipid-free, ready-made amino acid and glucose parenteral nutrition (PN) solution in dogs.</p></div></div>
<div class="section" id="vec12029-sec-0020" xmlns="http://www.w3.org/1999/xhtml"><h4>Design</h4><div class="para"><p>Retrospective study of dogs from 2006 to 2012 that received this form of PN.</p></div></div>
<div class="section" id="vec12029-sec-0030" xmlns="http://www.w3.org/1999/xhtml"><h4>Setting</h4><div class="para"><p>University veterinary teaching hospital.</p></div></div>
<div class="section" id="vec12029-sec-0040" xmlns="http://www.w3.org/1999/xhtml"><h4>Animals</h4><div class="para"><p>Seventy dogs presented to the hospital for treatment of various diseases in which PN was used as part of patient management. Dogs were administered PN at the discretion of the primary clinician.</p></div></div>
<div class="section" id="vec12029-sec-0050" xmlns="http://www.w3.org/1999/xhtml"><h4>Intervention</h4><div class="para"><p>A lipid-free, ready-made solution containing amino acid (59 g/L) and dextrose (100 g/L) was administered intravenously as a constant rate infusion to provide nutritional support.</p></div></div>
<div class="section" id="vec12029-sec-0060" xmlns="http://www.w3.org/1999/xhtml"><h4>Measurements and Main Results</h4><div class="para"><p>PN was provided for a median of 2.2 days (range 0.5–9.5 days) in the 70 dogs, totaling 168 days of PN. The PN provided a median of 5.5 g/100 kcal of protein (range 1–9.5 g/100 kcal) and a median of 2.2 mg/kg of bodyweight per minute (range 0.8–5.2 mg/kg/min) of glucose, which reflected a median of 57% of the resting energy requirement (range 9–100%). Metabolic complications developed in 43 of 67 dogs where these data were recorded, but the development of hyperkalemia was the only complication associated with a poor outcome (eg, death or euthanasia). Mechanical complications were seen in 28 dogs, and all but one of these occurred when PN was delivered through peripheral catheters. Septic complications were confirmed in 5 dogs.</p></div></div>
<div class="section" id="vec12029-sec-0070" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>This form of PN is suitable for clinical use and can provide both protein and calories to ill dogs. It was, however, associated with a high rate of complications and requires careful patient monitoring.</p></div></div>
]]></content:encoded><description>


Objective
To review the clinical use of a lipid-free, ready-made amino acid and glucose parenteral nutrition (PN) solution in dogs.


Design
Retrospective study of dogs from 2006 to 2012 that received this form of PN.


Setting
University veterinary teaching hospital.


Animals
Seventy dogs presented to the hospital for treatment of various diseases in which PN was used as part of patient management. Dogs were administered PN at the discretion of the primary clinician.


Intervention
A lipid-free, ready-made solution containing amino acid (59 g/L) and dextrose (100 g/L) was administered intravenously as a constant rate infusion to provide nutritional support.


Measurements and Main Results
PN was provided for a median of 2.2 days (range 0.5–9.5 days) in the 70 dogs, totaling 168 days of PN. The PN provided a median of 5.5 g/100 kcal of protein (range 1–9.5 g/100 kcal) and a median of 2.2 mg/kg of bodyweight per minute (range 0.8–5.2 mg/kg/min) of glucose, which reflected a median of 57% of the resting energy requirement (range 9–100%). Metabolic complications developed in 43 of 67 dogs where these data were recorded, but the development of hyperkalemia was the only complication associated with a poor outcome (eg, death or euthanasia). Mechanical complications were seen in 28 dogs, and all but one of these occurred when PN was delivered through peripheral catheters. Septic complications were confirmed in 5 dogs.


Conclusions
This form of PN is suitable for clinical use and can provide both protein and calories to ill dogs. It was, however, associated with a high rate of complications and requires careful patient monitoring.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12014" xmlns="http://purl.org/rss/1.0/"><title>Presumptive central nervous system cuterebriasis and concurrent protein-losing nephropathy in a dog</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12014</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Presumptive central nervous system cuterebriasis and concurrent protein-losing nephropathy in a dog</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Vincent J. Thawley, Jantra N. Suran, Elise M. Boller</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-01-30T14:39:23.418802-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/vec.12014</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/vec.12014</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12014</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Case Report</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="vec12014-sec-0010" xmlns="http://www.w3.org/1999/xhtml"><h4>Objective</h4><div class="para"><p>To describe the clinical course and successful management of a dog suspected to have central nervous system (CNS) <em>Cuterebra</em> larval migration and concurrent protein-losing nephropathy (PLN).</p></div></div>
<div class="section" id="vec12014-sec-0020" xmlns="http://www.w3.org/1999/xhtml"><h4>Case Summary</h4><div class="para"><p>A 1-year-old castrated male mixed breed dog was diagnosed with presumptive CNS cuterebriasis based on history, progressively deteriorating mentation, seizures, and magnetic resonance images showing a tubular lesion consistent with a migrating <em>Cuterebra</em> tract. Additionally, serum biochemistry and urine analyses revealed the development of a severe PLN. Surgical removal of the <em>Cuterebra</em> was attempted unsuccessfully, and subsequently, the dog was treated with ivermectin, antihistamines, anticonvulsants, and a tapering dose of glucocorticoids. Over several weeks the dog's neurologic status improved and the PLN resolved completely.</p></div></div>
<div class="section" id="vec12014-sec-0030" xmlns="http://www.w3.org/1999/xhtml"><h4>New or Unique Information Provided</h4><div class="para"><p>This case describes successful management of presumptive CNS cuterebriasis in a dog. It is also, to our knowledge, the first report of PLN associated with cuterebriasis in the veterinary literature.</p></div></div>
]]></content:encoded><description>


Objective
To describe the clinical course and successful management of a dog suspected to have central nervous system (CNS) Cuterebra larval migration and concurrent protein-losing nephropathy (PLN).


Case Summary
A 1-year-old castrated male mixed breed dog was diagnosed with presumptive CNS cuterebriasis based on history, progressively deteriorating mentation, seizures, and magnetic resonance images showing a tubular lesion consistent with a migrating Cuterebra tract. Additionally, serum biochemistry and urine analyses revealed the development of a severe PLN. Surgical removal of the Cuterebra was attempted unsuccessfully, and subsequently, the dog was treated with ivermectin, antihistamines, anticonvulsants, and a tapering dose of glucocorticoids. Over several weeks the dog's neurologic status improved and the PLN resolved completely.


New or Unique Information Provided
This case describes successful management of presumptive CNS cuterebriasis in a dog. It is also, to our knowledge, the first report of PLN associated with cuterebriasis in the veterinary literature.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12039" xmlns="http://purl.org/rss/1.0/"><title>Veterinary nephrology – Yesterday and today</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12039</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Veterinary nephrology – Yesterday and today</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Stephen P. DiBartola</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-04-08T07:11:24.051082-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/vec.12039</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/vec.12039</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12039</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Editorial</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">111</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">114</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[]]></content:encoded><description/></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12030" xmlns="http://purl.org/rss/1.0/"><title>Renal pathophysiology: lessons learned from the canine remnant kidney model</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12030</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Renal pathophysiology: lessons learned from the canine remnant kidney model</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Scott A. Brown</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-06T12:44:05.469663-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/vec.12030</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/vec.12030</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12030</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">State of the Art Review</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">115</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">121</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="vec12030-sec-0010" xmlns="http://www.w3.org/1999/xhtml"><h4>Objective</h4><div class="para"><p>To review the pathophysiology of chronic kidney disease (CKD) in dogs and the contributions of the canine remnant kidney model to our understanding of this disease.</p></div></div>
<div class="section" id="vec12030-sec-0020" xmlns="http://www.w3.org/1999/xhtml"><h4>Data Sources</h4><div class="para"><p>Original studies in the human and veterinary medical fields.</p></div></div>
<div class="section" id="vec12030-sec-0030" xmlns="http://www.w3.org/1999/xhtml"><h4>Data Synthesis</h4><div class="para"><p>Three of the fundamental principles of modern nephrology—the intact nephron hypothesis, the trade-off hypothesis, and the hyperfiltration theory were developed directly as a result of studies of the remnant kidney model. Most of the pivotal early studies were conducted in dogs. As a result, our understanding of CKD, and of the renal and systemic adaptations to CKD, is largely based on studies of this model.</p></div></div>
<div class="section" id="vec12030-sec-0040" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Studies of the remnant kidney model have advanced our understanding of the pathophysiology of CKD. Nearly every therapeutic intervention used in CKD, by veterinarians and physicians alike, has its basis in studies of the remnant kidney model or in knowledge that was derived from studies of this model. A great debt is owed to the canine participants in these studies and to a small number of key scientists who conducted this important and insightful research.</p></div></div>
]]></content:encoded><description>


Objective
To review the pathophysiology of chronic kidney disease (CKD) in dogs and the contributions of the canine remnant kidney model to our understanding of this disease.


Data Sources
Original studies in the human and veterinary medical fields.


Data Synthesis
Three of the fundamental principles of modern nephrology—the intact nephron hypothesis, the trade-off hypothesis, and the hyperfiltration theory were developed directly as a result of studies of the remnant kidney model. Most of the pivotal early studies were conducted in dogs. As a result, our understanding of CKD, and of the renal and systemic adaptations to CKD, is largely based on studies of this model.


Conclusions
Studies of the remnant kidney model have advanced our understanding of the pathophysiology of CKD. Nearly every therapeutic intervention used in CKD, by veterinarians and physicians alike, has its basis in studies of the remnant kidney model or in knowledge that was derived from studies of this model. A great debt is owed to the canine participants in these studies and to a small number of key scientists who conducted this important and insightful research.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12032" xmlns="http://purl.org/rss/1.0/"><title>The role of phosphorus in the pathophysiology of chronic kidney disease</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12032</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">The role of phosphorus in the pathophysiology of chronic kidney disease</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Rebecca F. Geddes, Natalie C. Finch, Harriet M. Syme, Jonathan Elliott</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-06T12:44:19.412144-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/vec.12032</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/vec.12032</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12032</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">State of the Art Review</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">122</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">133</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="vec12032-sec-0010" xmlns="http://www.w3.org/1999/xhtml"><h4>Objective</h4><div class="para"><p>To review the human and veterinary literature on the role of phosphorus in the pathophysiology of chronic kidney disease (CKD) and to explore why control of plasma phosphorus concentration is an important goal in the management of patients with this disease.</p></div></div>
<div class="section" id="vec12032-sec-0020" xmlns="http://www.w3.org/1999/xhtml"><h4>Data Sources</h4><div class="para"><p>Human and veterinary studies, reviews, clinical reports, textbooks, and recent research findings focused on phosphate homeostasis and CKD patient management.</p></div></div>
<div class="section" id="vec12032-sec-0030" xmlns="http://www.w3.org/1999/xhtml"><h4>Human Data Synthesis</h4><div class="para"><p>Recent studies using rodent models and human patients with CKD have focused on trying to elucidate the role of the phosphatonins, predominantly fibroblast growth factor-23, in phosphate homeostasis and the pathophysiology of secondary renal hyperparathyroidism (SRHP). Fibroblast growth factor-23 is now considered to be a key regulator of plasma phosphorus concentration in people but has only recently been investigated in companion animal species.</p></div></div>
<div class="section" id="vec12032-sec-0040" xmlns="http://www.w3.org/1999/xhtml"><h4>Veterinary Data Synthesis</h4><div class="para"><p>Cross-sectional studies of naturally occurring CKD in dogs and cats have shown hyperphosphatemia and SRHP to be highly prevalent and associated with increased morbidity and mortality in these patients. Experimental studies of surgically induced renal impairment in the dog and cat, and cases of naturally occurring CKD have emphasized the ability of renal care diets to modify plasma phosphorus and parathyroid hormone concentrations. Evidence from these studies indicates that maintaining plasma phosphorus concentrations to within the International Renal Interest Society targets for CKD patients improves survival time and reduces clinical manifestations of hyperphosphatemia and SRHP.</p></div></div>
<div class="section" id="vec12032-sec-0050" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>The maintenance of plasma phosphorus concentrations in to within the International Renal Interest Society targets is recommended in management of CKD patients. The discovery of the phosphatonins has improved understanding of the mechanisms involved in phosphorus homeostasis and SRHP and may lead to improved ability to monitor and manage these patients.</p></div></div>
]]></content:encoded><description>


Objective
To review the human and veterinary literature on the role of phosphorus in the pathophysiology of chronic kidney disease (CKD) and to explore why control of plasma phosphorus concentration is an important goal in the management of patients with this disease.


Data Sources
Human and veterinary studies, reviews, clinical reports, textbooks, and recent research findings focused on phosphate homeostasis and CKD patient management.


Human Data Synthesis
Recent studies using rodent models and human patients with CKD have focused on trying to elucidate the role of the phosphatonins, predominantly fibroblast growth factor-23, in phosphate homeostasis and the pathophysiology of secondary renal hyperparathyroidism (SRHP). Fibroblast growth factor-23 is now considered to be a key regulator of plasma phosphorus concentration in people but has only recently been investigated in companion animal species.


Veterinary Data Synthesis
Cross-sectional studies of naturally occurring CKD in dogs and cats have shown hyperphosphatemia and SRHP to be highly prevalent and associated with increased morbidity and mortality in these patients. Experimental studies of surgically induced renal impairment in the dog and cat, and cases of naturally occurring CKD have emphasized the ability of renal care diets to modify plasma phosphorus and parathyroid hormone concentrations. Evidence from these studies indicates that maintaining plasma phosphorus concentrations to within the International Renal Interest Society targets for CKD patients improves survival time and reduces clinical manifestations of hyperphosphatemia and SRHP.


Conclusions
The maintenance of plasma phosphorus concentrations in to within the International Renal Interest Society targets is recommended in management of CKD patients. The discovery of the phosphatonins has improved understanding of the mechanisms involved in phosphorus homeostasis and SRHP and may lead to improved ability to monitor and manage these patients.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12036" xmlns="http://purl.org/rss/1.0/"><title>Calcitriol, calcidiol, parathyroid hormone, and fibroblast growth factor-23 interactions in chronic kidney disease</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12036</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Calcitriol, calcidiol, parathyroid hormone, and fibroblast growth factor-23 interactions in chronic kidney disease</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Joao F. Brito Galvao, Larry A. Nagode, Patricia A. Schenck, Dennis J. Chew</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-04-08T07:11:24.051082-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/vec.12036</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/vec.12036</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12036</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">State of the Art Review</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">134</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">162</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="vec12036-sec-0010" xmlns="http://www.w3.org/1999/xhtml"><h4>Objective</h4><div class="para"><p>To review the inter-relationships between calcium, phosphorus, parathyroid hormone (PTH), parent and activated vitamin D metabolites (vitamin D, 25(OH)-vitamin D, 1,25(OH)<sub>2</sub>-vitamin D, 24,25(OH)<sub>2</sub>-vitamin D), and fibroblast growth factor-23 (FGF-23) during chronic kidney disease (CKD) in dogs and cats.</p></div></div>
<div class="section" id="vec12036-sec-0020" xmlns="http://www.w3.org/1999/xhtml"><h4>Data Sources</h4><div class="para"><p>Human and veterinary literature.</p></div></div>
<div class="section" id="vec12036-sec-0030" xmlns="http://www.w3.org/1999/xhtml"><h4>Human Data Synthesis</h4><div class="para"><p>Beneficial effects of calcitriol treatment during CKD have traditionally been attributed to regulation of PTH but new perspectives emphasize direct renoprotective actions independent of PTH and calcium. It is now apparent that calcitriol exerts an important effect on renal tubular reclamation of filtered 25(OH)-vitamin D, which may be important in maintaining adequate circulating 25(OH)-vitamin D. This in turn may be vital for important pleiotropic actions in peripheral tissues through autocrine/paracrine mechanisms that impact the health of those local tissues.</p></div></div>
<div class="section" id="vec12036-sec-0040" xmlns="http://www.w3.org/1999/xhtml"><h4>Veterinary Data Synthesis</h4><div class="para"><p>Limited information is available reporting the benefit of calcitriol treatment in dogs and cats with CKD.</p></div></div>
<div class="section" id="vec12036-sec-0050" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>A survival benefit has been shown for dogs with CKD treated with calcitriol compared to placebo. The concentrations of circulating 25(OH)-vitamin D have recently been shown to be low in people and dogs with CKD and are related to survival in people with CKD. Combination therapy for people with CKD using both parental and activated vitamin D compounds is common in human nephrology and there is a developing emphasis using combination treatment with activated vitamin D and renin-angiotensin-aldosterone-system (RAAS) inhibitors.</p></div></div>
]]></content:encoded><description>


Objective
To review the inter-relationships between calcium, phosphorus, parathyroid hormone (PTH), parent and activated vitamin D metabolites (vitamin D, 25(OH)-vitamin D, 1,25(OH)2-vitamin D, 24,25(OH)2-vitamin D), and fibroblast growth factor-23 (FGF-23) during chronic kidney disease (CKD) in dogs and cats.


Data Sources
Human and veterinary literature.


Human Data Synthesis
Beneficial effects of calcitriol treatment during CKD have traditionally been attributed to regulation of PTH but new perspectives emphasize direct renoprotective actions independent of PTH and calcium. It is now apparent that calcitriol exerts an important effect on renal tubular reclamation of filtered 25(OH)-vitamin D, which may be important in maintaining adequate circulating 25(OH)-vitamin D. This in turn may be vital for important pleiotropic actions in peripheral tissues through autocrine/paracrine mechanisms that impact the health of those local tissues.


Veterinary Data Synthesis
Limited information is available reporting the benefit of calcitriol treatment in dogs and cats with CKD.


Conclusions
A survival benefit has been shown for dogs with CKD treated with calcitriol compared to placebo. The concentrations of circulating 25(OH)-vitamin D have recently been shown to be low in people and dogs with CKD and are related to survival in people with CKD. Combination therapy for people with CKD using both parental and activated vitamin D compounds is common in human nephrology and there is a developing emphasis using combination treatment with activated vitamin D and renin-angiotensin-aldosterone-system (RAAS) inhibitors.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12026" xmlns="http://purl.org/rss/1.0/"><title>Lyme nephritis</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12026</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Lyme nephritis</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Meryl P. Littman</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-05T10:58:32.259547-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/vec.12026</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/vec.12026</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12026</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">State of the Art Review</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">163</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">173</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="vec12026-sec-0010" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Objective</h4><div class="para"><p>To review what is known and highlight knowledge gaps regarding Lyme nephritis (LN).</p></div></div>
<div class="section" id="vec12026-sec-0020" xmlns="http://www.w3.org/1999/xhtml"><h4>Data Sources</h4><div class="para"><p>Publications identified via PubMed using the keywords “<em>Borrelia burgdorferi</em>,” “Borreliosis,” “glomerulonephritis,” “protein-losing nephropathy,” “autoimmunity,” and “retriever,” and as generated by investigators working in the fields of Borreliosis and immune-mediated glomerulonephritis.</p></div></div>
<div class="section" id="vec12026-sec-0030" xmlns="http://www.w3.org/1999/xhtml"><h4>Human Data Synthesis</h4><div class="para"><p>Postborrelial immune-mediated glomerulonephritis was described recently in 6 people; 3 responded to antimicrobials/steroids, 1 to antimicrobials/angiotensin-converting enzyme inhibitor/warfarin, 1 required hemodialysis but became hemodialysis independent after 5 months and treatment with antimicrobials, steroids, plasmapheresis, immunoglobulin, and 1 did not respond to steroids and angiotensin-converting enzyme inhibitor and still requires hemodialysis.</p></div></div>
<div class="section" id="vec12026-sec-0040" xmlns="http://www.w3.org/1999/xhtml"><h4>Veterinary Data Synthesis</h4><div class="para"><p>Lyme nephritis is seen in &lt;1–2% of Lyme seropositive dogs, with an average onset at 5–6 years. Labrador and Golden Retrievers are predisposed to this condition. Prior or concurrent lameness is described in 9–28% cases. Historical presentations include acute progressive protein-losing nephropathy with membranoproliferative glomerulonephritis, tubular necrosis/regeneration, and interstitial nephritis, but possibly milder forms exist. Complications include thromboembolic events, hypertension, effusive disease, and oliguric/anuric renal failure. Diagnostic tests help stage disease and rule out other causes. Renal biopsy is advocated early, when intervention may help, and to prove if immune-complex disease exists. Treatment includes standard therapy for protein-losing nephropathy, long-term antimicrobials, and perhaps immunosuppressive therapy.</p></div></div>
<div class="section" id="vec12026-sec-0050" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>There is no experimental model of LN to study predisposing factors, pathogenesis, onset, progression, treatment, or prevention. There are no predictive tests to identify the few individuals at highest risk, therefore all seropositive dogs should be screened and monitored for proteinuria. Lyme nephritis mimics other forms of protein-losing nephropathy and sometimes Leptospirosis. Renal biopsy helps show if immune-complex disease exists, but may not prove LN specifically. More studies are warranted on dogs with Lyme-specific immune-complex deposition to evaluate risk factors, understand pathogenesis, variability of expression, and to validate treatment and prevention protocols.</p></div></div>
]]></content:encoded><description>

Objective
To review what is known and highlight knowledge gaps regarding Lyme nephritis (LN).


Data Sources
Publications identified via PubMed using the keywords “Borrelia burgdorferi,” “Borreliosis,” “glomerulonephritis,” “protein-losing nephropathy,” “autoimmunity,” and “retriever,” and as generated by investigators working in the fields of Borreliosis and immune-mediated glomerulonephritis.


Human Data Synthesis
Postborrelial immune-mediated glomerulonephritis was described recently in 6 people; 3 responded to antimicrobials/steroids, 1 to antimicrobials/angiotensin-converting enzyme inhibitor/warfarin, 1 required hemodialysis but became hemodialysis independent after 5 months and treatment with antimicrobials, steroids, plasmapheresis, immunoglobulin, and 1 did not respond to steroids and angiotensin-converting enzyme inhibitor and still requires hemodialysis.


Veterinary Data Synthesis
Lyme nephritis is seen in &lt;1–2% of Lyme seropositive dogs, with an average onset at 5–6 years. Labrador and Golden Retrievers are predisposed to this condition. Prior or concurrent lameness is described in 9–28% cases. Historical presentations include acute progressive protein-losing nephropathy with membranoproliferative glomerulonephritis, tubular necrosis/regeneration, and interstitial nephritis, but possibly milder forms exist. Complications include thromboembolic events, hypertension, effusive disease, and oliguric/anuric renal failure. Diagnostic tests help stage disease and rule out other causes. Renal biopsy is advocated early, when intervention may help, and to prove if immune-complex disease exists. Treatment includes standard therapy for protein-losing nephropathy, long-term antimicrobials, and perhaps immunosuppressive therapy.


Conclusions
There is no experimental model of LN to study predisposing factors, pathogenesis, onset, progression, treatment, or prevention. There are no predictive tests to identify the few individuals at highest risk, therefore all seropositive dogs should be screened and monitored for proteinuria. Lyme nephritis mimics other forms of protein-losing nephropathy and sometimes Leptospirosis. Renal biopsy helps show if immune-complex disease exists, but may not prove LN specifically. More studies are warranted on dogs with Lyme-specific immune-complex deposition to evaluate risk factors, understand pathogenesis, variability of expression, and to validate treatment and prevention protocols.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12027" xmlns="http://purl.org/rss/1.0/"><title>Familial renal disease in soft-coated wheaten terriers</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12027</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Familial renal disease in soft-coated wheaten terriers</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Shelly L. Vaden, Meryl P. Littman, Rachel E. Cianciolo</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-05T10:58:45.683758-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/vec.12027</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/vec.12027</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12027</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">State of the Art Review</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">174</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">183</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="vec12027-sec-0010" xmlns="http://www.w3.org/1999/xhtml"><h4>Objective</h4><div class="para"><p>To review what is known about the familial renal diseases in soft-coated wheaten terriers (SCWT), provide an update in developments in this field including the relationship with protein-losing nephropathy (PLN) and the potential association with protein-losing enteropathy (PLE).</p></div></div>
<div class="section" id="vec12027-sec-0020" xmlns="http://www.w3.org/1999/xhtml"><h4>Data Sources</h4><div class="para"><p>Information was derived from studies of dogs maintained in the North Carolina State University colony, information contained within an open registry of affected dogs, and data gathered from the general population of wheaten terriers at risk as well as studies performed on banked DNA samples from affected SCWT in the general population and normal geriatric dogs seen at the University of Pennsylvania (PennVet).</p></div></div>
<div class="section" id="vec12027-sec-0030" xmlns="http://www.w3.org/1999/xhtml"><h4>Human Data Synthesis</h4><div class="para"><p>A two-hit pathogenesis has been proposed in some types of human focal segmental glomerulosclerosis, specifically the subset of cases that are associated with a podocytopathy. At risk podocytes may be predisposed to injury by disease processes that would be reversible in other patients.</p></div></div>
<div class="section" id="vec12027-sec-0040" xmlns="http://www.w3.org/1999/xhtml"><h4>Veterinary Data Synthesis</h4><div class="para"><p>Mutations were found in association with PLN in SCWT, indicating a podocytopathy that causes a change in glomerular permselectivity. This podocytopathy leads to the development of lesions resembling focal segmental glomerulosclerosis. There is also strong evidence supporting a high prevalence of food hypersensitivity reactions in SCWT, although it is unclear if these reactions have a primary or secondary role in the development of PLE. There are also suggestions of immunodysregulation in affected SCWT.</p></div></div>
<div class="section" id="vec12027-sec-0050" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>PLN in SCWT is due to a podocytopathy. The cause of PLE has not been identified; however, it is possible that PLE develops from a functional-structural abnormality in the intestines and food allergies develop as secondary phenomena. It is also possible that inflammatory events that are the result of either immunodysregulation or food allergies might lead to the development of PLE. In either case, PLE most likely exacerbates PLN in affected SCWT.</p></div></div>
]]></content:encoded><description>


Objective
To review what is known about the familial renal diseases in soft-coated wheaten terriers (SCWT), provide an update in developments in this field including the relationship with protein-losing nephropathy (PLN) and the potential association with protein-losing enteropathy (PLE).


Data Sources
Information was derived from studies of dogs maintained in the North Carolina State University colony, information contained within an open registry of affected dogs, and data gathered from the general population of wheaten terriers at risk as well as studies performed on banked DNA samples from affected SCWT in the general population and normal geriatric dogs seen at the University of Pennsylvania (PennVet).


Human Data Synthesis
A two-hit pathogenesis has been proposed in some types of human focal segmental glomerulosclerosis, specifically the subset of cases that are associated with a podocytopathy. At risk podocytes may be predisposed to injury by disease processes that would be reversible in other patients.


Veterinary Data Synthesis
Mutations were found in association with PLN in SCWT, indicating a podocytopathy that causes a change in glomerular permselectivity. This podocytopathy leads to the development of lesions resembling focal segmental glomerulosclerosis. There is also strong evidence supporting a high prevalence of food hypersensitivity reactions in SCWT, although it is unclear if these reactions have a primary or secondary role in the development of PLE. There are also suggestions of immunodysregulation in affected SCWT.


Conclusions
PLN in SCWT is due to a podocytopathy. The cause of PLE has not been identified; however, it is possible that PLE develops from a functional-structural abnormality in the intestines and food allergies develop as secondary phenomena. It is also possible that inflammatory events that are the result of either immunodysregulation or food allergies might lead to the development of PLE. In either case, PLE most likely exacerbates PLN in affected SCWT.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12031" xmlns="http://purl.org/rss/1.0/"><title>Kidney diseases caused by glomerular basement membrane type IV collagen defects in dogs</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12031</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Kidney diseases caused by glomerular basement membrane type IV collagen defects in dogs</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">George E. Lees</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-06T12:44:11.129416-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/vec.12031</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/vec.12031</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12031</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">State of the Art Review</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">184</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">193</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="vec12031-sec-0010" xmlns="http://www.w3.org/1999/xhtml"><h4>Objective</h4><div class="para"><p>To review the pathogenesis, as well as the clinical and pathologic features of canine glomerular diseases caused by genetic type IV collagen defects.</p></div></div>
<div class="section" id="vec12031-sec-0020" xmlns="http://www.w3.org/1999/xhtml"><h4>Data Sources</h4><div class="para"><p>Original studies and review articles from human and veterinary medical fields.</p></div></div>
<div class="section" id="vec12031-sec-0030" xmlns="http://www.w3.org/1999/xhtml"><h4>Human Data Synthesis</h4><div class="para"><p>Presence in glomerular basement membranes (GBM) of a network composed of α3.α4.α5 heterotrimers of type IV collagen is required to maintain structure and function of glomerular capillary walls.</p></div></div>
<div class="section" id="vec12031-sec-0040" xmlns="http://www.w3.org/1999/xhtml"><h4>Veterinary Data Synthesis</h4><div class="para"><p>Hereditary nephropathy (HN) is the most commonly used name for kidney diseases that occur in dogs due to genetic type IV collagen abnormalities. To date, 4 different collagen IV gene mutations have been identified in dogs with HN; 2 are <em>COL4A5</em> mutations that cause X-linked HN (XL-HN), and 2 are <em>COL4A4</em> mutations that cause autosomal recessive HN (AR-HN). Affected males with XL-HN and affected males and females with AR-HN develop juvenile-onset kidney disease manifested by proteinuria typically starting at 3–6 months of age and followed by progressive kidney disease leading to terminal failure usually at 6–24 months of age. Carrier female dogs with XL-HN also develop proteinuria starting at 3–6 months of age, but progressive disease causing kidney failure is uncommon until they are &gt;5 years old. The distinctive pathologic lesions of HN are extensive multilaminar splitting and thickening of the GBM, as demonstrated by electron microscopy, and abnormal type IV collagen α-chain content of basement membranes, as demonstrated by immunolabeling. Identification of the underlying gene mutations has permitted genetic testing and selective breeding practices that currently are minimizing HN in breeds known to be at risk.</p></div></div>
<div class="section" id="vec12031-sec-0050" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Canine HN is a rare disease that should be considered whenever a dog exhibits a juvenile-onset kidney disease characterized partly by proteinuria, but highly specialized methods are required to pursue a definitive diagnosis.</p></div></div>
]]></content:encoded><description>


Objective
To review the pathogenesis, as well as the clinical and pathologic features of canine glomerular diseases caused by genetic type IV collagen defects.


Data Sources
Original studies and review articles from human and veterinary medical fields.


Human Data Synthesis
Presence in glomerular basement membranes (GBM) of a network composed of α3.α4.α5 heterotrimers of type IV collagen is required to maintain structure and function of glomerular capillary walls.


Veterinary Data Synthesis
Hereditary nephropathy (HN) is the most commonly used name for kidney diseases that occur in dogs due to genetic type IV collagen abnormalities. To date, 4 different collagen IV gene mutations have been identified in dogs with HN; 2 are COL4A5 mutations that cause X-linked HN (XL-HN), and 2 are COL4A4 mutations that cause autosomal recessive HN (AR-HN). Affected males with XL-HN and affected males and females with AR-HN develop juvenile-onset kidney disease manifested by proteinuria typically starting at 3–6 months of age and followed by progressive kidney disease leading to terminal failure usually at 6–24 months of age. Carrier female dogs with XL-HN also develop proteinuria starting at 3–6 months of age, but progressive disease causing kidney failure is uncommon until they are &gt;5 years old. The distinctive pathologic lesions of HN are extensive multilaminar splitting and thickening of the GBM, as demonstrated by electron microscopy, and abnormal type IV collagen α-chain content of basement membranes, as demonstrated by immunolabeling. Identification of the underlying gene mutations has permitted genetic testing and selective breeding practices that currently are minimizing HN in breeds known to be at risk.


Conclusions
Canine HN is a rare disease that should be considered whenever a dog exhibits a juvenile-onset kidney disease characterized partly by proteinuria, but highly specialized methods are required to pursue a definitive diagnosis.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12028" xmlns="http://purl.org/rss/1.0/"><title>Extracorporeal renal replacement therapy and blood purification in critical care</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12028</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Extracorporeal renal replacement therapy and blood purification in critical care</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Larry D. Cowgill, Julien Guillaumin</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-20T08:55:47.241128-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/vec.12028</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/vec.12028</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12028</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">State of the Art Review</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">194</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">204</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="vec12028-sec-0010" xmlns="http://www.w3.org/1999/xhtml"><h4>Objective</h4><div class="para"><p>To review indications methods of renal replacement therapies (RRT) and practical considerations for the creation of a RRT program.</p></div></div>
<div class="section" id="vec12028-sec-0020" xmlns="http://www.w3.org/1999/xhtml"><h4>Data Sources</h4><div class="para"><p>Current human and veterinary literature review with a focus on advanced renal physiology and clinical experience in RRT and acute/chronic kidney diseases.</p></div></div>
<div class="section" id="vec12028-sec-0030" xmlns="http://www.w3.org/1999/xhtml"><h4>Data Synthesis</h4><div class="para"><p>Renal replacement therapies encompass intermittent hemodialysis, continuous renal replacement therapy as well as some “hybrid” techniques. Each method of RRT has practical and theoretical advantages but currently there is no evidence that one technique is superior to the other.</p></div></div>
<div class="section" id="vec12028-sec-0040" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>RRT is a valuable therapeutic tool for treatment of acute kidney injury and chronic kidney disease. The implementation of an RRT program needs to take into consideration multiple parameters beyond the choice of an RRT platform.</p></div></div>
]]></content:encoded><description>


Objective
To review indications methods of renal replacement therapies (RRT) and practical considerations for the creation of a RRT program.


Data Sources
Current human and veterinary literature review with a focus on advanced renal physiology and clinical experience in RRT and acute/chronic kidney diseases.


Data Synthesis
Renal replacement therapies encompass intermittent hemodialysis, continuous renal replacement therapy as well as some “hybrid” techniques. Each method of RRT has practical and theoretical advantages but currently there is no evidence that one technique is superior to the other.


Conclusions
RRT is a valuable therapeutic tool for treatment of acute kidney injury and chronic kidney disease. The implementation of an RRT program needs to take into consideration multiple parameters beyond the choice of an RRT platform.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12034" xmlns="http://purl.org/rss/1.0/"><title>Evidence-based step-wise approach to managing chronic kidney disease in dogs and cats</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12034</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Evidence-based step-wise approach to managing chronic kidney disease in dogs and cats</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">David J. Polzin</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-07T15:45:33.791226-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/vec.12034</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/vec.12034</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12034</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Clinical Practice Review</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">205</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">215</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="vec12034-sec-0010" xmlns="http://www.w3.org/1999/xhtml"><h4>Objective</h4><div class="para"><p>To provide a framework for successfully managing chronic kidney disease (CKD) over an extended period of time with the goal of optimizing clinical outcomes by fostering a veterinarian-client relationship that facilitates successful application of evidence-based treatment.</p></div></div>
<div class="section" id="vec12034-sec-0020" xmlns="http://www.w3.org/1999/xhtml"><h4>Etiology</h4><div class="para"><p>Ultimately, CKD results from loss of functional nephrons; however, the specific disease process responsible for this loss usually cannot be determined due to development of chronic changes (eg, fibrosis) and compensatory adaptations that have occurred in the kidneys of patients with CKD. Earlier diagnosis may foster a better understanding of the etiologies of CKD.</p></div></div>
<div class="section" id="vec12034-sec-0030" xmlns="http://www.w3.org/1999/xhtml"><h4>Diagnosis</h4><div class="para"><p>Diagnosis of CKD is based on establishing loss of kidney function(s) due to primary kidney disease that have been present for an extended time (typically 3 months or longer).</p></div></div>
<div class="section" id="vec12034-sec-0040" xmlns="http://www.w3.org/1999/xhtml"><h4>Therapy</h4><div class="para"><p>The goals of therapy are to: (1) slow progressive loss of kidney function, (2) ameliorate clinical and biochemical consequences of CKD, and (3) maintain adequate nutrition. These goals are achieved by: (1) managing adaptive processes that promote progression of CKD, (2) controlling intake of water, nutrients, minerals and electrolytes, and (3) correcting hormonal deficiencies.</p></div></div>
<div class="section" id="vec12034-sec-0050" xmlns="http://www.w3.org/1999/xhtml"><h4>Prognosis</h4><div class="para"><p>The short-term prognosis for dogs with CKD varies from good to poor, while the long-term prognosis for dogs with CKD is generally guarded to poor depending on the International Renal Interest Society (IRIS) CKD stage of the patient. Both short-term and long-term prognosis for cats with CKD may vary from good to poor depending on the IRIS CKD stage. However, prognosis is more variable and unpredictable in cats.</p></div></div>
]]></content:encoded><description>


Objective
To provide a framework for successfully managing chronic kidney disease (CKD) over an extended period of time with the goal of optimizing clinical outcomes by fostering a veterinarian-client relationship that facilitates successful application of evidence-based treatment.


Etiology
Ultimately, CKD results from loss of functional nephrons; however, the specific disease process responsible for this loss usually cannot be determined due to development of chronic changes (eg, fibrosis) and compensatory adaptations that have occurred in the kidneys of patients with CKD. Earlier diagnosis may foster a better understanding of the etiologies of CKD.


Diagnosis
Diagnosis of CKD is based on establishing loss of kidney function(s) due to primary kidney disease that have been present for an extended time (typically 3 months or longer).


Therapy
The goals of therapy are to: (1) slow progressive loss of kidney function, (2) ameliorate clinical and biochemical consequences of CKD, and (3) maintain adequate nutrition. These goals are achieved by: (1) managing adaptive processes that promote progression of CKD, (2) controlling intake of water, nutrients, minerals and electrolytes, and (3) correcting hormonal deficiencies.


Prognosis
The short-term prognosis for dogs with CKD varies from good to poor, while the long-term prognosis for dogs with CKD is generally guarded to poor depending on the International Renal Interest Society (IRIS) CKD stage of the patient. Both short-term and long-term prognosis for cats with CKD may vary from good to poor depending on the IRIS CKD stage. However, prognosis is more variable and unpredictable in cats.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12033" xmlns="http://purl.org/rss/1.0/"><title>A clinical review of pathophysiology, diagnosis, and treatment of uroabdomen in the dog and cat</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12033</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">A clinical review of pathophysiology, diagnosis, and treatment of uroabdomen in the dog and cat</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Jennifer R. Stafford, Joseph W. Bartges</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-07T15:45:29.929687-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/vec.12033</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/vec.12033</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12033</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Clinical Practice Review</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">216</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">229</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="vec12033-sec-0010" xmlns="http://www.w3.org/1999/xhtml"><h4>Objective</h4><div class="para"><p>To review current literature regarding uroabdomen in dogs and cats with respect to etiology, diagnostic approach, medical and surgical treatment, and prognosis.</p></div></div>
<div class="section" id="vec12033-sec-0020" xmlns="http://www.w3.org/1999/xhtml"><h4>Etiology</h4><div class="para"><p>Uroabdomen in dogs and cats is most often associated with vehicular or blunt trauma. This condition may also result from urinary tract obstruction, traumatic bladder expression or catheterization, neoplasia, and postoperative leakage following abdominal or urogenital surgery.</p></div></div>
<div class="section" id="vec12033-sec-0030" xmlns="http://www.w3.org/1999/xhtml"><h4>Diagnosis</h4><div class="para"><p>Disruption to the urinary tract should be considered when a patient is diagnosed with azotemia, hyperkalemia, and abdominal effusion. By comparing the creatinine concentration of the abdominal fluid to the serum or plasma creatinine concentration, a diagnosis of uroabdomen can be made if the creatinine ratio is ≥2:1. In most patients imaging studies with contrast are necessary to identify the exact source of urine leakage and to determine therapeutic options.</p></div></div>
<div class="section" id="vec12033-sec-0040" xmlns="http://www.w3.org/1999/xhtml"><h4>Therapy</h4><div class="para"><p>Uroabdomen is a medical emergency, not a surgical emergency. Acute management involves stabilization of the patient with IV fluid therapy and treatment of hyperkalemia. Urinary diversion and, in some cases, peritoneal dialysis are necessary to stabilize the patient until life-threatening conditions such as hyperkalemia or concomitant injuries such as pulmonary contusions resolve. Once the patient is stable for anesthesia, surgical repair, if indicated, may be performed.</p></div></div>
<div class="section" id="vec12033-sec-0050" xmlns="http://www.w3.org/1999/xhtml"><h4>Prognosis</h4><div class="para"><p>The prognosis of patients with uroabdomen depends on the extent of urinary and nonurinary injuries as well as the development of complications. Potential complications include dehiscence or urine leakage following surgical repair of the urinary tract, urosepsis, unresolving azotemia secondary to renal damage or underlying renal insufficiency, or stricture formation in the urinary tract.</p></div></div>
]]></content:encoded><description>


Objective
To review current literature regarding uroabdomen in dogs and cats with respect to etiology, diagnostic approach, medical and surgical treatment, and prognosis.


Etiology
Uroabdomen in dogs and cats is most often associated with vehicular or blunt trauma. This condition may also result from urinary tract obstruction, traumatic bladder expression or catheterization, neoplasia, and postoperative leakage following abdominal or urogenital surgery.


Diagnosis
Disruption to the urinary tract should be considered when a patient is diagnosed with azotemia, hyperkalemia, and abdominal effusion. By comparing the creatinine concentration of the abdominal fluid to the serum or plasma creatinine concentration, a diagnosis of uroabdomen can be made if the creatinine ratio is ≥2:1. In most patients imaging studies with contrast are necessary to identify the exact source of urine leakage and to determine therapeutic options.


Therapy
Uroabdomen is a medical emergency, not a surgical emergency. Acute management involves stabilization of the patient with IV fluid therapy and treatment of hyperkalemia. Urinary diversion and, in some cases, peritoneal dialysis are necessary to stabilize the patient until life-threatening conditions such as hyperkalemia or concomitant injuries such as pulmonary contusions resolve. Once the patient is stable for anesthesia, surgical repair, if indicated, may be performed.


Prognosis
The prognosis of patients with uroabdomen depends on the extent of urinary and nonurinary injuries as well as the development of complications. Potential complications include dehiscence or urine leakage following surgical repair of the urinary tract, urosepsis, unresolving azotemia secondary to renal damage or underlying renal insufficiency, or stricture formation in the urinary tract.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12035" xmlns="http://purl.org/rss/1.0/"><title>Current techniques in peritoneal dialysis</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12035</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Current techniques in peritoneal dialysis</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Linda A. Ross, Mary Anna Labato</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-04-08T07:11:24.051082-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/vec.12035</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/vec.12035</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fvec.12035</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Clinical Practice Review</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">230</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">240</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="vec12035-sec-0010" xmlns="http://www.w3.org/1999/xhtml"><h4>Objective</h4><div class="para"><p>To provide a current overview of the technique of peritoneal dialysis in dogs and cats.</p></div></div>
<div class="section" id="vec12035-sec-0020" xmlns="http://www.w3.org/1999/xhtml"><h4>Clinical Implication</h4><div class="para"><p>Peritoneal dialysis is the process by which water and solutes move between blood in the peritoneal capillaries and fluid (dialysate) instilled into the peritoneal cavity, across the semipermeable membrane of the peritoneum. The primary indication for peritoneal dialysis (PD) in animals is for treatment of renal failure to correct water, solute, and acid-base abnormalities and to remove uremic toxins.</p></div></div>
<div class="section" id="vec12035-sec-0030" xmlns="http://www.w3.org/1999/xhtml"><h4>Summary</h4><div class="para"><p>Peritoneal dialysis is a modality of renal replacement therapy commonly used in human medicine for the treatment of chronic kidney disease and end-stage kidney failure. Peritoneal dialysis utilizes the peritoneum as a membrane across which fluids and uremic solutes are exchanged. Dialysate is instilled into the peritoneal cavity and, through the process of diffusion and osmosis, water, toxins, electrolytes, and other small molecules are allowed to equilibrate.</p></div></div>
]]></content:encoded><description>


Objective
To provide a current overview of the technique of peritoneal dialysis in dogs and cats.


Clinical Implication
Peritoneal dialysis is the process by which water and solutes move between blood in the peritoneal capillaries and fluid (dialysate) instilled into the peritoneal cavity, across the semipermeable membrane of the peritoneum. The primary indication for peritoneal dialysis (PD) in animals is for treatment of renal failure to correct water, solute, and acid-base abnormalities and to remove uremic toxins.


Summary
Peritoneal dialysis is a modality of renal replacement therapy commonly used in human medicine for the treatment of chronic kidney disease and end-stage kidney failure. Peritoneal dialysis utilizes the peritoneum as a membrane across which fluids and uremic solutes are exchanged. Dialysate is instilled into the peritoneal cavity and, through the process of diffusion and osmosis, water, toxins, electrolytes, and other small molecules are allowed to equilibrate.

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