pancreatitis
V Marchettia*, E Goria, I Lippia, E Luchettia, ML Mancab and A Pierinia.
aVeterinary Teaching Hospital “Mario Modenato”, Department of Veterinary Sciences, University of Pisa, via Livornese Lato monte, San Piero a Grado 56122, Pisa, Italy.
bDepartment of Clinical and Experimental Medicine, University of Pisa, Italy.
*Corresponding author: Veronica Marchetti, e-mail: veronica.marchetti@unipi.it; Phone: +39 050 2210100.
Abstract
Objective To evaluate prognostic factors for canine acute pancreatitis based on clinical and laboratory data that can be easily assessed in veterinary practice.
Design Retrospective study between January 2010 and December 2013.
Methods The diagnosis of acute pancreatitis was based on clinical signssymptoms signs and an abnormalpositivity to SNAP® cPL™ test resultabnormal SNAP® cPL™ SNAP cPL test result, concurrently with an ultrasound pattern suggestive of pancreatitis. Dogs were divided into survivors and non-survivors. Twelve clinical and laboratory parameters were evaluated: respiratory rate, rectal temperature, WBC, HCT, total serum proteins, albumin, creatinine, cholesterol, total and ionizedzed calcium, sodium, and potassium. Clinical and clinicopathological data were statistically compared between survivors and non-survivors. A value of p <0.05 was considered significant and a value of p <0.01 as highly significant. The odds ratio (OR) was calculated.
Results Fifty client-owned dogs with a diagnosis of AP were enrolled. Serum creatinine (p 0.017) and sodium (p 0.004) correlated significantly with the outcome. Serum sodium < 139.0 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25
mmol/L (139.0 mEq/L), and serum creatinine > 212 μmol/L (2.4 mg/dL) were associated significantly with poor prognosis. Azotemia (OR 12.5; CI: 1.32-118.48) and hyponatremia (OR 4.9; CI: 1.36-17.64) were associated with increased risk of death.
Conclusions In dogs with acute pancreatitis, hyponatremia and azotemia seem to be significantly associated with an increased risk of death.
Key words: acute pancreatitis; dog; hyponatremia; azotemia; prognosis. Abbreviations
AKI acute kidney injury AP acute pancreatitis
In veterinary medicine, acute pancreatitis (AP) is a relatively frequent pathological condition. Although AP is generally regarded as a significant illness in dogs, its actual incidence is unknown. Some dogs have subclinical or mild disease, and recover within a few days without specific treatment. However, others show more severe forms, which may result in death, if not promptly recognised and treated.1,2 An early assessment of disease severity and the identification of risk factors, is thus essential for the appropriate management of AP.2
Scoring systems based on the careful monitoring of patients in an intensive care unit are commonly used in human medicine.3-6 The acute physiology and chronic health evaluation system (APACHE) is considered as the most sensitive model, able to make prognosis within the first 24 hours, with an accuracy of 90%. Clinical parameters included in the APACHE classification system are: body temperature, mean arterial pressure, heart and respiratory rate, oxygen partial pressure, arterial pH, sodium and potassium ions, serum creatinine, HCT and WBC. 7 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49
In veterinary medicine, two recent studies evaluated the prognosis and outcome of AP in dogs. Mansfield et al.developed a clinical severity index to report the outcome in dogs with an ultrasound or histological diagnosis of AP. An elevated clinical severity index score was associated with higher mortality. 8
The outcome of dogs with AP was also evaluated by Pápa, where hypothermia and metabolic acidosis correlated significantly with poor prognosis.2
The aim of the present study was to evaluate prognostic factors for canine AP based exclusively on clinical and laboratory data that can be easily assessed in veterinary practice. Materials and Methods
For the present study an evaluation of the database of all dogs admitted to the University Teaching Hospital between January 2010 and December 2013, was performed, in order to identify dogs with AP. The diagnosis of AP was based on the following criteria: (1) two or more of the following clinical signs: abdominal pain, polyuria/polydipsia, diarrhoea, vomiting or anorexia/dysorexia for fewer than 7 days, (2) ultrasound evidence of AP (Xario XG ultrasound unit, Toshiba, Tokyo, Japan) without other identifiable diseases and (3) abnormal SNAP® cPL™ test(Idexx Laboratories, Milan, Italy).
Ultrasound findings associated with pancreatic inflammation vary with the severity and chronicity of the disease. Decreased echogenicity in AP reflects oedema, haemorrhage and necrosis, while the surrounding fat is generally moderately hyperechoic. When significantly enlarged, the right lobe of the pancreas may move from its normal position, dorsal or dorso-medial to the duodenum, to lie dorso-laterally. The stomach or duodenum may become distended with fluid, showing wall thickening and lack of peristalsis, due to functional ileus. Changes in the pancreas may be accompanied by localised or generalised accumulation of peritoneal effusion. Severe pancreatitis can also result in generalised peritoneal effusion. The pancreatic duct may be dilated and become as wide as the pancreatic-duodenal vein.9
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Dogs were included in the study if the following 12 parameters were available: respiratory rate, rectal temperature, WBC, HCT, total serum proteins, albumin, creatinine, cholesterol, total and ionic calcium, sodium, and potassium. CBC (Procyte DX, Idexx Laboratories, Milan, Italy), serum biochemistry profile (Liasys, Assel srl, Guidonia-Montecelio, Rome, Italy) and electrolytes (Stat Profile pHOx Series Analyzers, Nova Biomedical, Waltham, US) were performed by automated clinical analysers.
The following were excluded from the study: dogs with a previous diagnosis of AP, chronic kidney disease, diabetes mellitus, hypothyroidism, hypoadrenocorticism, hyperadrenocorticism, or dogs with pancreatic neoplasia.
Dogs were divided in two groups: survivors and non-survivors. Non-survivors included dogs that had died within seven days of hospital admission. Clinical and clinicopathological data were compared between survivors and non-survivors.
Cut-off values for serum creatinine and sodium were taken from the highest values in the survivor group. Table 2 shows cut-off values of serum sodium < 139.0 mmol/L (139.0 mEq/L), and serum creatinine > 212 μmol/L (2.4 mg/dL). Odds Ratio (OR) was calculated using these cut-offs. Data were analysed with the Mann Whitney test using Statgraphics Plus 5.1 (Manugistic Inc., Rockville, MD, US). A value of p <0.05 was considered significant, and a value of p <0.01 as highly significant.
Results
Forty-eight dogs, 20 males, (18 intact, 2 neutered), and 28 females, (19 intact, 9 spayed) of several breeds were enrolled. The mean age was 9.2 + 3.8 years.
The most commonly involved breeds were mixed breeds (14 dogs), Dachshund (3), Beagle (3), Siberian Husky (3), Yorkshire Terrier (3), Boxer (2), Labrador Retriever (2), German Shepard (2), English Setter (2), and 14 other breeds comprising the remaining 14 dogs.
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At clinical examination 43/48 dogs (89.6%) showed depression, anorexia/dysorexia, weight loss, nausea or vomiting and diarrhoea. In addition to clinical signs of AP, three patients (3/48, 6.2%) showed respiratory distress, one patient showed ascites (2%), one showed jaundice, and one showed hypovolemic shock.
Table 1 reports the reference range, mean value and standard deviation for the 12 clinical and laboratory parameters.
Seventeen of forty-eight dogs (35.4%) died within the first 48 hours.
Serum creatinine and sodium were statistically associated with outcome in canine AP, p 0.017 and p 0.004, respectively (Table 1). The remaining parameters (respiratory rate, temperature, HCT, WBC, total protein, albumin, cholesterol, total calcium, calcium, and potassium) did not show a significant difference between the survivor and non-survivor groups. The presence of a left shift in the neutrophil count was present in 13 dogs (27%), but was not associated with the outcome.
Table 3 shows the OR values. In table 3 cut-off values of serum sodium < 139.0 mmol/L ([139.0 mEq/L], and serum creatinine > 212 μmol/L ([2.4 mg/dL] were used. Azotemia (OR 12.5; CI: 1.32-118.48) and hyponatremia (OR 4.9; CI: 1.36-17.64) were associated with an increased risk of death.
Discussion
This study concurrently used clinical signs (anorexia, lethargy, abdominal pain, vomiting), ultrasound findings and abnormal SNAP® cPL™ test resultsSNAP cPL SNAP cPL positivity as inclusion criteria for canine AP, as reported in a recent work.10
The Nowadays, SNAP® cPL™ test is considered as the most sensitive and specific marker of AP in dogs.11,12 To the best of our knowledge, only one research group has used the SNAP® cPL ™ SNAP cPL SNAP cPLtest, abdominal ultrasound and clinicopathological findings at the same time as inclusion criteria for AP.10
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Beall et al demonstrated that the SNAP® cPL™ agrees with the Spec cPL test: 96-100% in normal canine serum samples with normal levels of cPL, and 88-92% for samples with an elevated cPL.13
In the Pápa study, a diagnosis of AP was based on the simultaneous presence of clinical signs of AP, increased activity of serum amylase or lipase, ultrasonographic and/or macroscopic appearance and cytological or histological evidence of AP.2 Serum amylase and lipase have been reported to have a low sensitbivility (50% and 71%, respectively11) and low specificity (50% and 43%, respectively11). However, in 2008, Steiner showed no correlation between elevated levels of lipase or amylase and canine AP.14
Mansfield proposed a clinical severity index for canine AP.8 The diagnosis of AP was made on the basis of an abdominal ultrasound or histological examination. Although, abdominal ultrasound is reported to have a moderate sensibility (68%15), no clear data are available regarding the specificity.
However, abdominal ultrasound alone, based on purely morphological criteria, cannot unequivocally identify a mild or recent inflammatory condition, in which anatomical changes have not yet occurred.1,9,16 Although pancreatic biopsy and histopathologic examination are the best options for a diagnosis of AP, they still have a limited feasibility in clinical practice.1,14
A recent study, performed in dogs with clinical signs of acute abdominal disease (≥ 2 of the following clinical signs: acute (< 2 days) onset of abdominal pain, vomiting, abdominal distension, or diarrhea), highlighted the sensitivity (82%) and specificity (59%) of the SNAP® cPL™ test.17 Therefore, a positive SNAP® cPL™ test result may provide a "false positive" diagnosis for AP in up to 40% of dogs presenting abdominal pain.17 The specificity of the SNAP® cPL™ test decreases to 45% in dogs with hyperadrenocorticism, which showed positive abnormal results, without clinical signs suggestive of AP.18 The inclusion criteria and 124 125 126 127 128 129 130 131 132 133 134 135 136 137 138 139 140 141 142 143 144 145 146 147 148
the use of multiple diagnostic modalities may have increased the significance of the results in the present study.
It would be useful to identify a wide range of prognostic factors, possibly including clinical signs and laboratory parameters commonly altered during canine AP.1,16,19 In the present study, the choice of 12 variables was based on physiopathological mechanisms that occur during canine AP: respiratory rate, rectal temperature, WBC, total serum protein and serum albumin are influenced by the magnitude of the inflammation; serum creatinine concentration is associated with various degrees of hydration and, possibly, with pre-renal azotemia; total calcium and ionized calcium concentration may occur in peripancreatic fat saponification.20 Cholesterol disorders may be a cause or a consequence of AP20, while sodium and potassium levels are influenced by gastrointestinal loss, kidney injury and inflammation.21,22
Dogs with chronic kidney disease, diabetes mellitus, hypothyroidism, hypoadrenocorticism, and hyperadrenocorticism, or dogs with a final diagnosis of pancreatic neoplasia were excluded because all these diseases could be associated with AP and with abnormal SNAP® cPL SNAP™ cPL test results. They could also influence the clinical signs, mortality rate and laboratory parameters considered in this study.
In the present study, alterations in serum creatinine and sodium showed significant riskwere identified as significant factors of poor outcome in dogs with pancreatitis. Hypothermia at the time of admission was not associated with a negative outcome: this result is not in agreement with a previous study.2 Moreover, theThe remaining other parameters (respiratory rate, temperature, HCT, WBC, total protein, albumin, cholesterol, total calcium, calcium, potassium) did not correlate with a poor prognosis.
In our study, OR values of serum creatinine and sodium support the positive association between azotemia and negative outcome or hyponatremia and negative outcome (Table 23). 149 150 151 152 153 154 155 156 157 158 159 160 161 162 163 164 165 166 167 168 169 170 171 172
In canine AP azotemiaAzotemia has been reported as a prognostic marker in canine AP. Mansfield found that dogs with a renal damage score of 2 (anuria or azotemia >1.5-fold increase in serum urea and creatinine concentration) had a higher mortality than dogs with a renal damage score of 0 or 1. However, as the renal damage score was part of a multi-organ clinical severity index, azotemia was not directly associated with prognosis.8 In another study, azotemia was present in 55% of dogs with AP, but was not considered to be of prognostic significanceinterest.2 Indeed, in human medicine, acute kidney injury (AKI) is a common complication of severe pancreatitis, which increases the risk of mortality.23-25 AKI can be the result of hypoxemia, oxidative stress, decrease in renal perfusion and hypovolemia due to AP.25 The use of serum (symmetric dimethylarginine, SDMA)26 and urinary markers27 (i.e. albumin, -glutamyl transferase) of AKI would have been helpful to identify patients with pre-clinical grades od AKI.
During AP, hyponatremia can occur due to gastrointestinal loss, peritoneal effusion, kidney injury and systemic inflammatory response syndrome.28,29
In our study, 89.6% of dogs showed vomiting or diarrhoea, therefore, gastrointestinal loss was the most probable cause of hyponatremia. Gut barrier damage could have played a prognostic role in our dogs due to a possible bacterial translocation.30
The This study has several limitations. First, the lack of histopathology. Secondly, it would have been interesting to assess urinary output and natriuresis, as serum sodium is influenced by renal excretion and anuric/oliguric patients had a worse outcome.31 28 Although, patients with endocrine disorders were excluded from the study, it is not possible to affirm that patients who showed early mortality did not have pre-clinical stages of endocrine disorders. Finally, although all the dogs in the present study received a similar medical management, the AP therapy included analgesia with opioid drugs, fluid therapy, antiemetic drugs, such as maropitant, and anti-acids, such as ranitidine or omeprazole. No dogs received fresh frozen 173 174 175 176 177 178 179 180 181 182 183 184 185 186 187 188 189 190 191 192 193 194 195 196 197
plasma infusion. The effects of different drugs and dosages on mortality were not considered by the authors.
In conclusion, the present study has examined the prognostic parameters in canine AP, which can be easily assessed in veterinary clinical practice. At the time of diagnosisadmission, the assessment of serum sodium and serum creatinine may be helpful in evaluating the risk of death.
Acknowledgments
The authors wish to thank Dr. Ilaria Ficini for her technical assistance. References
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Table 1: Clinical and laboratory parameter values evaluated in the 48 patients.
Parameters All patients
(mean ± SD) Survivors (mean ± SD) Non survivors (mean ± SD) Reference interval Respiratory rate (Bpm) 35 ± 15 33 ± 14 39 ± 18 10-30 Temperature (°C) 38.4 ± 0.8 38.6 ± 0.7 38.1 ± 0.9 37.0–39.0 Hct (%) 39.5 ± 9.4 40.9 ± 9.1 36.8 ± 9.7 37.3–61.7 WBC (K/µL) 19.35 ± 13.5 17.17 ± 10.99 23.33 ± 16.81 5.05–16.75 Total protein g/L 60 ± 14 62 ± 12 56 ± 17 55-77 Albumin g/L 27 ± 7 28 ± 7 27 ± 8 25–40 Creatinine μmol/L A 168 ± 274 97.2 ± 53.0 291.7 ± 442.0 70-132 Cholesterol mmol/L 6.1 ± 3.3 6.2 ± 3.2 6.0 ± 3.5 3.9–6.9 Total calcium mmol/L 2.4 ± 0.4 2.4 ± 0.4 2.3 ± 0.4 2.0–3.0 Calcium mmol/L 1.11 ± 0.17 1.14 ± 0.14 1.06 ± 0.20 1.12–1.42 Sodium mmol/L B 139.9 ± 5.7 141.6 ± 4.4 136.8 ± 6.6 146.0–156.0 Potassium mmol/L 4.2 ± 1.0 4.1 ± 0.8 4.5 ± 1.4 3.9–5.5 A p 0.017 B p 0.004 289 290 291 292
Table 2: Clinical and laboratory results of thirty-one surviving dogs and 17 nonsurviving dogs using Mann-Whitney U test.
Parameters Non survivors (mean ± SD) Survivors (mean ± SD)
Respiratory rate (bpm) 39 ± 18 33 ± 14 Temperature (°C) 38.1 ± 0.9 38.6 ± 0.7 Hct (%) 36.8 ± 9.7 40.9 ± 9.1 WBC (K/µL) 23.33 ± 16.81 17.17 ± 10.99 Total protein g/L 56 ± 17 62 ± 12 Albumin g/L 27 ± 8 28 ± 7 Creatinine μmol/L A 291.7 ± 442.0 97.2 ± 53.0 Cholesterol mmol/L 6.0 ± 3.5 6.2 ± 3.2
Total calcium mmol/L 2.3 ± 0.4 2.4 ± 0.4
Calcium mmol/L 1.06 ± 0.20 1.14 ± 0.14 Sodium mmol/LB 136.8 ± 6.6 141.6 ± 4.4 Potassium mmol/L 4.5 ± 1.4 4.1 ± 0.8 A p 0.017 B p 0.004 293 294 295 296 297
Table 2: OR values
Parameters Non survivors Survivors OR CI (95%)
Creatinine μmol/L ≥ 212 5 1 12.50A 1.32 – 118.48
Creatinine μmol/L < 212 12 30
Sodium mmol/L ≤ 139.0 10 7 4.90B 1.36 – 17.64
Sodium mmol/L >139.0 7 24
OR, Odds Ratio; CI, Confidence Interval
A p 0.009 B p 0.012 298 299 300 301
