Materials and Methods

Case selection—Records of dogs that were evaluated at a primary emergency center (Murdoch Pet Emergency Centre) and a referral veterinary teaching hospital (Murdoch University Veterinary Teaching Hospital) in 1999 through 2006 and for which a diagnosis of pancreatitis was recorded were reviewed. Inclusion criteria included evidence of AP detected via abdominal ultrasonography or histologic examination of surgical or necropsy tissue samples, admission to hospital for treatment, complete daily clinical records (physical examination findings), and results of full clinicopathologic evaluation (hematologic and serum biochemical analyses and urinalysis as minimum) performed within 12 hours of admission. Ultrasonography was performed by a board-certified (or equivalent Australian qualification) radiologist. A diagnosis of AP was made if there was evidence of a large pancreas with patchy echogenicity or hyperechoic mesentery. Dogs were excluded if they were not admitted for treatment or were euthanatized for nonmedical reasons. Signalment, interval be- tween onset of clinical signs and evaluation, and interval from hospital admission until outcome (considered to be death or discharge from the hospital; designated as days until outcome) were recorded for each dog that fulfilled the inclusion criteria.

Development of the clinical severity index—Several body systems were evaluated in the dogs to develop an appropriate clinical severity index (Appendix). Abnormalities of the endocrine system (eg, diabetes mellitus or diabetic ketoacidosis) and hepatic system (eg, high serum activities of hepatocellular and cholestatic enzymes) were included and graded as part of the index on the basis of their inclusion in a previously published severity scheme.⁷ Other systems were included on the basis of criteria developed for critically ill patients¹⁵; these included the hematopoietic system to evaluate for signs of inflammation (high WBC count and moderate left-shift), development of systemic inflammatory syndrome (severe leukocytosis or leukopenia), or development of disseminated intravascular coagulation. Coagulation abnormalities included prolongation of prothrombin time, activated partial thromboplastin time, or activated clotting time and high plasma concentration of fibrinogen degradation products. Other critical care factors evaluated were the presence of cardiac arrhythmias (graded in ascending order according to whether relatively benign or potentially malignant), respiratory complications (graded in ascending order to reflect possible development of acute respiratory distress syndrome), renal disease (severe azotemia or anuria), and altered vascular forces (graded in ascending order to reflect changes in serum albumin concentration and systolic arterial blood pressure). On the basis of the human and veterinary medical literature, local pancreatic complications were also considered and included peritonitis that extended beyond the peripancreatic region and presence of a pancreatic pseudocyst or pancreatic abscess. Poor enteral health or altered intestinal integrity was also graded if there was poor intestinal motility (defined as an absence of intestinal sounds during ≥ 3 auscultations of the left and right sides of the abdomen during a 24-hour period), development of regurgitation (presumed to be the result of reflux esophagitis), altered intestinal integrity (evidence of bleeding into gastrointestinal tract, such as melena or hematochezia), or a prolonged period of anorexia (> 3 days), regardless of whether this was prior to or during hospitalization.

Each of these scored factors was evaluated for significance (ie, whether it contributed to survival) by use of a Pearson χ² and Fisher exact test; a value of P < 0.05 was considered significant. Factors were retained for evaluation if they were significant. A clinical score index based on the significant factors was determined for each dog by assessment of the medical record data collected within the first 24-hour period after admission to the hospital. An organ score based on clinicopathologic variables was also calculated for each dog from laboratory information obtained within the first 24-hour period after admission to the hospital, according to a previously published method.⁷ In that organ scoring scheme, 1 point is allocated for abnormalities associated with the leukogram (> 10% band neutrophils or WBC > 24 × 10⁹ cells/L), kidneys (serum urea concentration > 14 mmol/L [39.2 mg/dL] and serum creatinine concentration > 300 μmol/L [3.3 mg/dL]), liver (serum alanine transferase activity > 240 U/L, serum aspartate aminotransferase activity > 240 U/L, or serum alkaline phosphatase activity > 420 U/L), acid-base buffering (blood bicarbonate concentration > 26 mmol/L or < 13 mmol/L or anion gap < 15 mmol/L or > 38 mmol/L), and the endocrine pancreas (blood glucose concentration > 13 mmol/L [234 mg/dL] or serum β-hydroxybutyrate concentration > 1 mmol/L). The total number of points that could be allocated to a dog by use of this initial scoring system was 24.

Serum C-RP concentration measurement—During a 3-month period, dogs admitted to Murdoch University Veterinary Teaching Hospital or Murdoch Pet Emergen- cy Centre that had a diagnosis of AP (confirmed via ultrasonographic or histologic evaluation of the pancreas) were also evaluated prospectively. The dogs were admitted and treated as considered appropriate by attending veterinarians, and none were euthanatized for nonmedical reasons. Severity index scores were determined as described, and treatment data were recorded. From each dog, a blood sample (2 mL) was obtained via jugular or cephalic venipuncture within 24 hours after admission, with informed owner consent. Serum was harvested within 30 to 60 minutes of blood collection and frozen at −20°C; samples were then transported on dry ice, and C-RP concentration was measured by use of a solidphase sandwich immunoassay.^e,f The reference range for this assay in healthy dogs has been determined as 0 to 7.6 mg/L.^a

Statistical analysis—Correlation between the 2 severity scoring systems (the clinical severity index and clinicopathologic variable–based organ scoring scheme) and survival in all dogs was determined via Spearman rho calculation (a value of P < 0.05 was considered significant) and an ANOVA. Correlation between the 2 severity scoring systems and days until outcome in all cases was also determined by use of the Spearman rho (ρ; nonparametric) analysis because data were not distributed normally. Spearman rho analysis was also used to determine the correlation between serum C-RP concentration and each of the severity scoring schemes, between serum C-RP concentration determined within 2 days of onset of clinical signs and outcome (survival to discharge from the hospital or death), and between serum C-RP concentration determined at any time and outcome (survival to discharge from the hospital or death). For all analyses, a value of P < 0.05 was considered significant.

Results

Dogs—From the medical records, 68 dogs for which a diagnosis of pancreatitis had been made during the period of 1999 through 2006 were identified. Sixty-one dogs fulfilled the inclusion criteria and were admitted for treatment; in 12 of these dogs, serum C-RP concentration was measured. Seven dogs were excluded because they were euthanatized due to financial reasons alone or had incomplete medical records. In the study group, there were 36 females (of which 35 were spayed and 1 was sexually intact) and 25 males (of which 17 were neutered and 8 were sexually intact). Mean age of all dogs was 8.5 years (range, 1 to 16 years). Breeds included Terrier breeds (n = 12), Australian Kelpie or Australian Kelpie crossbreeds (8), Border Collie or Border Collie crossbreeds (7), Australian Cattle Dog (6), Bull Terrier (4), Miniature Schnauzer (3), Miniature Poodle (3), Rottweiler (2), Corgi (2), Golden Retriever (2), and Lhasa Apso (2). The other 10 dogs were mixed breeds.

Clinical severity index and organ scoring scheme— The medical records for each dog were reviewed, and the system factors used in the clinical severity index were assessed (Table 1). Statistical analysis of those data revealed an association between outcome and each of 4 body system classifications: the cardiac and respiratory system factors (P = 0.044 and P = 0.035, respectively), intestinal integrity (P = 0.009), and vascular forces (P = 0.003). There was no significant association between outcome and the renal, hematopoietic, hepatic, endocrine, or local complication factors; therefore, those classifications were excluded from the clinical severity index. Further evaluation of the local complication and hematopoietic systems also failed to identify a significant association between outcome and scores of 2 or 3 and 3 or 4, respectively. The remaining system, acid-base buffering, was not thoroughly assessed in our study because of a lack of consistent blood gas analysis among dogs during the study period. Therefore, in the final clinical severity index, the total maximum score was 10 points (maximum score of 2 for the cardiac, respiratory, and vascular forces systems and a maximum score of 4 for the intestinal integrity system).

Of the 61 dogs, 47 survived to discharge from the hospital and 14 died or were euthanatized for pancreatitis-associated medical reasons; the overall mortality rate was 23%. On the basis of scores (maximum of 10 points) derived by use of the clinical severity index, dogs were grouped into categories of 0, 1, 2, 3, 4, 5, and ≥ 6 scores (no score was > 6) and the outcomes for each category were examined (Figure 1). The numbers of dogs in each score category were 15 (24.6%), 15 (24.6%), 6 (9.8%), 8 (13.1%), 12 (19.7%), 4 (6.5%), and 1 (1.7%), respectively. The mortality rate for dogs that had a clinical severity index score ≥ 4 was 53%, compared with the overall mortality rate among all dogs of 23%. On the basis of the organ scoring scheme, dogs were grouped into categories of 0, 1, 2, 3, or 4 scores and the outcomes for each category were also examined. The numbers of dogs in each score category were 15 (24.6%), 17 (27.9%), 19 (31.1%), 7 (11.5%), and 3 (4.9%), respectively.

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Distribution of dogs with AP that survived to discharge from the hospital (black bars; n = 47) versus those that died or were euthanatized for reasons related to AP (gray bars; 14) according to scores derived by use of a clinical severity index (A) or an organ scoring scheme (B). The clinical severity index included assessments of factors associated with cardiovascular and respiratory systems, vascular forces, and intestinal integrity. The organ scoring scheme included assessments of clinicopathologic variables associated with the leukogram, kidneys, liver, endocrine pancreas, and acid-base buffering. For the clinical severity index, the maximum score was 10, although no dog received a score > 6; for the organ scoring scheme, the maximum score was 4.

Citation: Journal of the American Veterinary Medical Association 233, 6; 10.2460/javma.233.6.936

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The score derived by use of the clinical severity index had a significantly greater correlation with survival (ρ = −0.437; P = 0.000) than the score derived by use of the organ scoring scheme. Scores derived by use of the latter scheme had no significant correlation with outcome in the cohort of the present study (ρ = −0.096; P = 0.460). The mean score derived by use of the clinical severity index for the 47 survivors (1.62) was significantly (P = 0.000) lower than the mean score for the 14 dogs that died or were euthanatized (3.4). The ANOVA revealed that death was more likely to occur in dogs with higher clinical severity index scores. There was generally a fair degree of correlation within individuals between scores derived by both schemes; however, there were some outliers with poor correlation (Table 2). Six dogs had significantly lower organ scores, compared with their clinical severity index scores; 5 of these dogs died or were euthanatized as a result of their disease, and the dog that survived had a prolonged hospitalization period. There was a high rate of abnormalities in vascular forces or evidence of severely altered intestinal integrity in all 6 dogs (Table 3).

Among all 61 dogs, the mean ± SD interval from onset of clinical signs until outcome (ie, days until outcome, specifically death or discharge from the hospital) was 5.7 ± 3.12 (range, 1 to 15 days). Results of the ANOVA indicated that there was no significant (P = 0.329) difference in days until outcome between survivors (mean, 5.9 ± 3.23 days; range, 2 to 15; n = 47) and nonsurvivors (mean, 5.0 ± 2.69 days; range, 1 to 10; 14). However, there was a highly significant correlation (ρ = 0.554; P = 0.000) between the days until outcome and the clinical severity index score. There was also a significant correlation (ρ = 0.278; P = 0.03) between days until outcome and the organ score.

Assessment of serum C-RP concentration—In 12 dogs with AP, serum C-RP concentration was prospectively evaluated within 24 hours of hospital admission. Three of these dogs had hyperlipidemia at the time of sample collection. Concurrent diseases in this group included idiopathic epilepsy (n = 1), suspected hyperadrenocorticism (2), and atopic dermatitis that was controlled with prednisolone (2). All 12 dogs had high serum C-RP concentration; the mean ± SD value was 111.02 ± 103.93 mg/L (range, 24.2 to 374.51 mg/L [reference range, 0 to 7.6 mg/L]). There was poor correlation between serum C-RP concentration and scores derived by use of the clinical severity index (ρ = −0.057; P = 0.859) or organ scoring scheme (ρ = 0.026; P = 0.936). Although there was a slightly better correlation with the clinical severity index score, statistical significance was not reached. The mean C-RP concentration for survivors (89.2 ± 71.8 mg/L; range, 24.2 to 200.32 mg/mL; n = 9) did not differ significantly from the value for nonsurvivors (176.4 ± 173.9 mg/L; range, 48.8 to 374.51 mg/mL; 3). There was no significant correlation (ρ = −0.362; P = 0.247) between outcome and serum C-RP concentration. When serum C-RP concentration measured within 2 days of the onset of clinical signs and outcome were analyzed, findings for survivors and nonsurvivors differed significantly (mean serum C-RP concentration, 90.6 ± 75.2 mg/L; range, 26.77 to 200.32 mg/L [n = 7] and 374.5 mg/L [1], respectively; P = 0.012), but this difference did not represent a significant correlation between serum C-RP concentration and outcome (ρ = −0.577; P = 0.134).

Discussion

In dogs, the morbidity and mortality rates associated with AP are high.¹ In affected dogs, circulating pancreatic proteases are capable of inciting inflammation systemically, and subsequently, various free-radical, coagulation, complement, and kinin cascades can become activated.³ The generation of chemokines and cytokines leads to further tissue inflammation and injury, which in turn may cause multiorgan failure and death. In particular, IL-6, IL- 8, tumor necrosis factor-α, and C-RP have been associated with a poor prognosis in people with pancreatitis, whereas platelet-activating factor has been specifically implicated in the development of lung- associated injury.^16–18 Of these cytokines, it would appear that the circulating concentration of IL-6 has the best predictive value for organ failure in humans with severe pancreatitis.^17,19

In the present study, serum C-RP concentration was measured by use of an ELISA that was specific for canine C-RP and accurate for samples stored at temperatures less than −10°C for 3 months.^20,a For analysis of canine serum samples, the inter- and intra-assay coefficients of variation of the ELISA have been reported by the manufacturer^f as 8% and 6.7%, respectively. All 12 dogs in which serum C-RP concentration was measured in our study had values that were markedly greater than the upper limit of the established reference range; this finding is consistent with other data reported for other dogs with acute and chronic illnesses, including dogs with AP.^13,21-25,a-d None of the 12 dogs evaluated for C-RP concentration in our study had evidence of concurrent inflammatory or neoplastic disease with the exception of mild atopic dermatitis, and it would seem unlikely that atopic dermatitis would have contributed to the high serum C-RP concentration in the 2 affected dogs. Serum C-RP concentration is unaffected by treatment with prednisolone^26,c; thus, the administration of that drug to the 2 dogs with atopic dermatitis was unlikely to have altered the concentrations. Lipemia was detected in 3 of the 12 dogs in which serum C-RP concentration was assessed. Although lipemia can artifactually increase serum C-RP concentration, it has minimal impact on clinical interpretation of those values.^12,20

In the present study of dogs with AP, we failed to identify a correlation between serum C-RP concentration and outcome or clinical severity index score. This is in contrast to results of a study in which a difference in serum C-RP concentration between dogs with pancreatic necrosis (n = 9) and dogs with edematous pancreatic inflammation (5) was detected.^d A likely explanation for this disparity is that dogs in our study were probably more severely affected than the dogs evaluated in the previous study and would all likely have been classified in the pancreatic necrosis group. In another recent study,^b findings were similar to results of our study, in that although serum C-RP concentration was relatively increased in dogs with pancreatitis, all dogs that were critically ill had similar concentrations and it was not possible to differentiate between survivors and nonsurvivors on the basis of a single C-RP value. The reason that serum C-RP concentration may not correlate strongly to outcome may be dependent on the stage of the disease process during which the assessment was made. Serum concentration of C-RP sequentially decreases in dogs during treatment for pancreatitis¹³ and in humans with AP after 2 days from the onset of clinical signs.¹⁷ Serum C-RP concentration in samples that were obtained within 2 days of the onset of clinical signs had a greater correlation with outcome in the present study than did serum C-RP concentration measured in samples collected later, although fewer dogs were assessed. The delay between onset of clinical signs and admission to the hospital in our study appeared to be attributable to the facts that some dogs were treated by their veterinarians before being hospitalized and the owners of others did not seek veterinary care immediately. This period of delay probably provides a true representation of the attendant times of admission and diagnosis of AP at a veterinary hospital in the general dog population.

Although the number of dogs in which serum C-RP concentration was evaluated was small, the results of the present study suggested that assessment of this variable in dogs with AP at the earliest possible time should be considered in conjunction with application of a clinical severity index for AP in dogs, rather than as a stand-alone test, as a means to determine disease severity. However, if a serum sample is obtained within 2 days of the onset of clinical signs and serum C-RP concentration is high, then a poorer prognosis could be given. Sequential assessment of serum C-RP concentration may also be an effective and objective method for monitoring response to treatment.

Many clinical classification schemes for AP in humans have been assessed. The acute physiology, age, chronic health evaluation (APACHE) scheme, Ranson scheme, and Balthazar computed tomography severity index have been used with mixed results.^27–30 In humans, the development of pancreatic infection is considered the worst prognostic indicator, but such infections do not appear to typically develop in dogs with AP.^6,14,31 Clinical severity scoring schemes have been developed for assessment of inflammatory bowel disease in dogs and as a survival prediction index in dogs admitted to intensive care units, but the latter fails to take into account complications specific to pancreatitis.^15,32 A published severity scoring scheme for pancreatitis was calculated on clinicopathologic abnormalities determined from sample submissions to a clinical pathology laboratory.⁷ For purposes of that scheme, a diagnosis of pancreatitis was made solely on the basis of whether dogs had high serum lipase or amylase activity.⁷ As such, that scheme may have included dogs that did not truly have pancreatitis because the rate of falsepositive diagnosis associated with assessment of those biochemical variables alone is fairly high.² In our study, the mortality rate for dogs that were assigned a score of 3 or 4 by use of this clinicopathologic abnormality– based scheme was much lower than those reported in the original study.⁷ The reported mortality rate in the study involving the clinicopathologic scheme may also be inaccurate because of the possibility that dogs from which samples were derived did not have pancreatitis, as well as the possibility that some dogs that did have pancreatitis were excluded because the samples did not contain high serum lipase and amylase activities. Additionally, dogs that were euthanatized as a result of nonmedical reasons or that did not receive an optimal standard of care may have been included.⁷ In the present study, scores derived by use of the organ scoring scheme that was based on clinicopathologic variables were not significantly correlated with outcome (death or discharge from the hospital). Interestingly, scores for all but one of the organ systems evaluated for the organ score (ie, the endocrine pancreas, leukogram, and renal and hepatic systems) were not significantly associated with outcome in our study. The remaining system, acid-base buffering, was not thoroughly assessed in our study because of a lack of consistent blood gas analysis among dogs during the study period. The clinical severity index score had a significant correlation with outcome, although days until outcome was equally associated with severity by use of either classification scheme.

In humans, the development of severe peritonitis or infected pancreatic necroses is strongly indicative of a poor prognosis, whereas in dogs, pancreatic lesions (abscesses, acute fluid accumulations, or pseudocysts) have been similarly implicated.^33–35 Interestingly, among the 61 dogs with AP in the present study, local complications, even those considered severe, did not have an impact on outcome. This may reflect the large number of dogs (both survivors and nonsurvivors) that were recorded as having widespread peritonitis. Six dogs were recorded as having a score ≥ 2 in this category, and 5 of those dogs survived to discharge from the hospital; there was no significant association of scores ≥ 2 with outcome. This probably reflects both the low incidence of pancreatic abscess formation in dogs with AP and the recent trend in human gastroenterology toward conservative treatment of noninfected pancreatic lesions instead of surgical correction.^27–31 The 5 dogs with pancreatic pseudocysts or acute fluid accumulations that survived were all conservatively treated. Follow-up information was available for 3 of those dogs; in all, the original lesion had resolved within 4 to 6 months.

The development of systemic inflammatory response syndrome has also been identified as a strong indicator of poor prognosis in dogs with any illness, and diagnosis is often made on the basis of WBC abnormalities and high respiratory or heart rate.³⁶ Coagulation abnormalities were also included in our initial body system–based severity index because disseminated intravascular coagulation and thromboembolic complications are common and potentially devastating consequences of severe AP.^1,3,6 However, the hematopoietic complications initially considered (development of systemic inflammatory response syndrome or thromboembolic disease) were not correlated with survival in our study. This is despite strong links between these conditions and prognosis for other critical illnesses in dogs.^15,36 A large number of dogs in our study had abnormalities in the hematopoietic category, supporting the notion that all dogs with AP have some degree of inherent systemic inflammation. Stratification within the hematopoietic system category was also assessed, and thromboembolic disease (either overt or subclinical) was not significantly correlated with prognosis. Seven dogs had scores ≥ 3 in this category, and 5 of those dogs recovered. Causes of death of the 2 dogs that died were not recorded as potentially being attributable to thromboembolic complications; therefore, thromboembolic disease does not appear to play an important role in determination of AP severity in dogs.

Several factors may have contributed to the greater correlation of outcome with the scores derived by use of the clinical severity index developed in the present study, compared with findings in studies involving previously identified methods. What appears to be of most importance in dogs with AP is intestinal health, in particular during the period in which direct enteral nutrition is lacking, whether this is an intentional occurrence as part of the treatment or a disease-related complication. During starvation, inflammatory cytokines are produced by enterocytes and there is an increased incidence of bacterial translocation as a result of altered intestinal permeability, both of which are evident in naturally occurring AP in humans and experimentally induced AP in dogs.^37–43 Restoration or maintenance of intestinal health is of potentially great importance when developing treatment strategies for dogs with AP, and provision of enteral nutrition early in the disease process may prove to be a prime factor in treatment of dogs with this condition.

The clinical severity index established in the present study was developed to incorporate easily measurable variables that are most likely to contribute to the overall wellness of a dog with AP. Initial evaluation of this index revealed a significant negative correlation with outcome—as the clinical severity index score increased, the chance of survival decreased. A similar significant negative correlation with outcome was not identified for the organ scoring scheme. The strength of the clinical severity index, compared with the organ scoring scheme, was highlighted by the 6 dogs for which clinical severity index scores were high (mainly because of severely altered intestinal integrity or vascular forces) and poorly correlated with the organ scores. Without inclusion of factors relating to intestinal integrity or vascular forces, these dogs would have been assigned a low clinical severity index score indicative of mild disease; however, 5 of the 6 dogs died or were euthanatized as a result of their disease despite intensive treatment. Serum C-RP concentration was measured in 1 of these dogs, and that assessment alone would not have correlated with AP severity or outcome. Further analysis of additional dogs with AP from other veterinary hospitals may result in ongoing modification of the clinical severity index, eventually allowing devel- opment of the most robust system possible for severity assessment.

On the basis of sex and age distributions, the group of dogs evaluated in the present study was fairly similar to those evaluated in other studies^2,9,10 of pancreatitis in dogs, although the breed representation in our study may be geographically unique. Reported rates of mortality in dogs with AP range from 27% to 42%,^2,5,7,9,10 which suggests that the group of dogs in our study was representative of the general population of dogs with AP, that treatment was essentially appropriate, and that there was no preselection for the most severe cases (no dogs with chronic pancreatitis were knowingly included). The inclusion criteria in our study allowed dogs with ultrasonographic evidence of pancreatitis (with supportive clinical findings and clinicopathologic abnormalities) to be assessed. In 1 study,² the sensitivity of ultrasonography for diagnosis of pancreatitis in dogs was approximately 62%. Although this sensitivity is relatively low, dogs with acute and chronic pancreatitis were evaluated in the study²; thus, the true diagnostic value of ultrasonography in dogs with AP is probably much higher. In dogs, the typical ultrasonographic changes associated with AP include a large pancreas with a hypoechoic appearance and cavitary lesions, dilated pancreatic duct, and hyperechoic mesentery.^6,44–46 In comparison to the situation in humans, advanced imaging such as contrast medium–enhanced computed tomography may have no advantage over ultrasonography for the diagnosis of AP in dogs.⁴⁷ This likely reflects the fact that infected areas of pancreatic necrosis (for which computed tomography is considered the gold standard diagnostic tool) develop less frequently in dogs than in humans.³¹ In the present study, it is possible that some dogs with pancreatitis were evaluated at the hospital but were not included in the analyses because the diagnosis was not confirmed ultrasonographically. The rate of false-positive diagnosis of pancreatitis via ultrasonography is likely to be low with experienced operators, so it was assumed that all dogs that were included in our study did in fact have AP. The classification of pancreatitis is confusing and problematic, but in dogs and humans, it is assumed that the acute form involves some degree of necrosis.^1,14,48 Although ultrasonography cannot determine the cellular process within the pancreas, pancreatic neoplasia is considered unlikely in the dogs included in the present study because the outcome for each individual is known. Often the presence of pancreatic neoplasia is accompanied by pancreatic inflammation and necrosis; thus, the definitive differentiation of neoplasia and inflammation in the short term would have little bearing on our study results.⁶ Ultrasonography is also considered a highly sensitive technique for detection of pancreatic complications such as pseudocysts, acute fluid accumulations, or abscesses.^{6,33,44,49,50}

For dogs with AP, use of a clinical severity index, such as that developed in the present study, along with sequential measurement of serum C-RP concentration appears to be helpful in prognostic determination. Nevertheless, the clinical severity index score should not be used as the sole criterion on which treatment or prognosis in AP-affected dogs is determined at present because some dogs in our study that had high scores survived to discharge from the hospital and others that had lower scores died or were euthanatized. The clinical severity index may be useful in allowing multicenter comparison of treatments of dogs with severe naturally occurring AP. As new treatments based on an improved understanding of the pathophysiology of this disease are developed, use of this index may allow objective assessments of the usefulness of particular treatment options to be made.