The term HRS was originally defined as a fall from the second floor or higher that led to a triad of injuries, including epistaxis, hard palate fracture, and pneumothorax.1 On the basis of results of several studies,2–11,a veterinarians have a better understanding of HRS and some of the consequences that increase the risk of death for affected patients. Cats have the ability to survive falls that would be lethal to most humans because they have special biophysical principles2 (ie, gyroscopic righting reflex and limb flexing on landing). Following substantial falls, dogs generally sustain injuries to the vertebral column or long-bone fractures, whereas cats often sustain less severe injuries because they have a better ability to absorb the impact of the fall.3,7 Results of several studies3,5,8,10,a that involved cats with HRS indicate a positive association with the number or severity of injuries that cats sustained and the height of the fall and firmness of the landing surface. Common sequelae for cats after a substantial fall include shock, facial trauma, and thoracic and orthopedic injuries.5,8,10,a Abdominal injuries, including pancreatic trauma (ie, traumatic pancreatitis), have been infrequently reported in cats with HRS.4,6,12 In cats, blunt abdominal trauma may cause bruising and edema that can result in severe generalized pancreatitis, pancreatic necrosis, localized obstruction of pancreatic ducts, and peritonitis.13 In a study4 of 930 cats with HRS, 10 had traumatic pancreatitis as diagnosed via laparotomy and developed clinical signs such as anorexia and lethargy. Also in that study,4 of all the cats (n … 31) with abdominal trauma, pancreatic injuries were the most frequent, followed by bladder injuries. In another retrospective study11 of cats with HRS, 5 of 55 cats were identified as having pancreatic rupture over a 6-year period. Early diagnosis of traumatic pancreatitis is crucial to ensure rapid and appropriate treatment for affected patients.4,11
The clinical signs (anorexia, lethargy, and dehydration) associated with pancreatitis in cats are relatively nonspecific.14 The prevalence of pancreatitis in cats as determined via clinical methods varies substantially from that as determined via pathological methods,14–16 possibly because it is difficult to distinguish pancreatitis from other acute abdominal disorders clinically. Moreover, clinical signs associated with traumatic pancreatitis in cats with HRS are often delayed and may be masked by clinical signs associated with bruises, fractures, or pneumothorax. Traumatic pancreatitis is often undiagnosed in human patients after blunt trauma,17 and we assume it is the same for cats with HRS.
Methods for the diagnosis of traumatic pancreatitis are the same as those for diagnosis of acute pancreatitis caused by other etiologies. The current standard of care for antemortem diagnosis of traumatic pancreatitis in cats includes a high index of suspicion (ie, history of fall or blunt trauma), transabdominal ultrasonography, measurement of serum fPLI concentration, cytologic evaluation of pancreatic aspirates, and histologic evaluation of pancreatic biopsy specimens.18 However, pancreatic biopsies in cats with HRS are often contraindicated because those patients typically have multiple injuries, which make the administration of the anesthesia required for the biopsy inadvisable.
The use of minimally invasive diagnostic tests that measure serum fPLI concentration combined with abdominal ultrasonography has improved the sensitivity of identifying acute pancreatitis in cats.19–21 Measurement of serum fPLI concentration is both a sensitive and specific method for identifying cats with pancreatitis.18 Results of a study22 indicate that the use of a serum fPLI concentration ≥ 10 μg/L (reference range, 2.0 to 6.8 μg/L) as a cutoff for identifying cats with pancreatitis has a sensitivity of 67% (95% CI, 41% to 87%) and specificity of 91% (95% CI, 59% to 100%), whereas abdominal ultrasonography has a sensitivity of 67% (95% CI, 41% to 87%) and specificity of 73% (95% CI, 39% to 94%) for identifying cats with pancreatitis. In another studyb of 41 healthy cats and 141 cats with clinical signs of pancreatitis, the use of a serum fPLI concentration > 5.4 μg/L as a cutoff for identification of cats with pancreatitis had a sensitivity of 79% and a specificity of 82%. Thus, serum fPLI concentration is a clinically useful determinant for pancreatitis in cats.
The objectives of the study reported here were to evaluate the use of serum fPLI concentration and abdominal ultrasonography for identifying cats with traumatic pancreatitis. We hypothesized that the sensitivity of detecting cats with traumatic pancreatitis would be improved by the evaluation of serum fPLI concentration in combination with repeated abdominal ultrasonography (ie, twice within 48 hours after trauma).
Materials and Methods
Animals—Cats evaluated because of HRS at the Clinic of Surgery and Ophthalmology, University of Veterinary Medicine, Vienna, between March 1 and October 31, 2009, were considered for inclusion in the study. Most cats with HRS were initially examined at the hospital within 12 hours after the fall. Cats in the study included those whose owners confirmed seeing the patient fall from a second-floor (European-building standard) or higher (≥ 6 m [19.7 feet]) building or open window and those that were hospitalized for a minimum of 4 days. Cats excluded from the study included those that were unavailable for a second abdominal ultrasonographic examination because they had been discharged from the hospital, had surgery or died and those that had an increased serum creatinine (≥ 1.2 mg/dL; reference range, 0.4 to 1.2 mg/dL) or BUN (≥ 40 mg/dL; reference range, 20 to 40 mg/dL) concentration at initial examination because of the potential for an artificially increased serum fPLI concentration. Cats were also excluded from the study if they were not admitted to the hospital or were euthanized at the owner's request. For cats enrolled in the study, consent was obtained from the owners prior to study enrollment. All study procedures were evaluated and approved by the Institutional Animal Welfare and Ethics Committee of the University of Veterinary Medicine, Vienna.
Clinical examination and treatment—Information obtained for each cat included age, sex, breed, height from which the fall occurred, and date and time of the fall. Within 12 hours after hospital admission, each cat had a physical examination, radiographic examination of the thorax (and other parts of the body when indicated), CBC, and serum biochemical analysis performed. Treatment was administered to each cat at the discretion of the attending clinician and in accordance with physical examination and diagnostic findings.
Determination of serum fPLI concentration—From each cat, a blood sample (2 mL) was obtained from a jugular or cephalic vein during (within 12 hours after the fall) and at 24, 48, and 72 hours after the initial examination at the hospital. Within 30 to 60 minutes after blood sample collection, serum (0.5 mL) was removed from the blood samples and stored at −80°C until further analysis. The serum samples were shipped on dry ice to a university laboratoryc for determination of serum fPLI concentration via a commercially available assayd Serum fPLI concentrations > 5.4 μg/L were considered diagnostic for pancreatitis,b and each cat was classified as either having (serum fPLI concentration > 5.4 μg/L in at least 1 of the 4 samples) or not having (serum fPLI concentration < 5.4 μg/L in all 4 samples) pancreatitis.
Abdominal ultrasonography—Abdominal ultrasonography was performed with 1 of 2 ultrasound unitse,f and a 5- to 8-MHz curved-array small-parts transducer. Each cat was examined twice, at 24 to 48 hours and 72 to 96 hours after the initial physical examination, with at least 48 hours between the first and second ultrasonographic examinations. The ultrasonographic examinations were performed by various radiologists, but all sonograms were evaluated by 1 veterinary radiologist (KMH) to obtain a diagnosis for the present study. Pancreatic and peripancreatic abnormalities suspected to be associated with HRS included hypoechoic or heteroechoic pancreatic parenchyma, pancreatic enlargement, hyperechoic mesentery, and peritoneal effusion. For each evaluation, a cat was assigned 1 point for each abnormality that was present, and a cumulative score ≥ 3 was considered suggestive of traumatic pancreatitis.
Evaluation of cats after discharge from hospital—Two to 3 weeks after each cat was discharged from the hospital, its owner was contacted via telephone by an investigator (EZ). Each owner was asked questions regarding the cat's food intake, general behavior and activity, and whether the cat had been examined by another veterinarian since being discharged from the hospital to assess whether the cat had developed clinical signs of acute pancreatitis after it was discharged from the hospital.
Statistical analysis—A Spearman coefficient of rank correlation was calculated to assess the association between serum fPLI concentration and blood sample collection time. Mean serum fPLI concentration was compared between cats with and without pancreatitis via an ANOVA for repeated measures. The difference between the cumulative scores for the first and second abdominal ultrasonographic examinations was evaluated with a Pearson χ2 test. A kappa coefficient (κ) was calculated to evaluate the extent of agreement beyond chance between serum fPLI concentration and abdominal ultrasonography for the diagnosis of traumatic pancreatitis in cats with HRS. All analyses were performed with statistical software,g and values of P < 0.05 were considered significant.
Results
Animals—Of the 94 cats with HRS that were examined at the hospital between March 1 and October 31, 2009, 34 met the inclusion criteria for and were enrolled in the study. The cats enrolled in the study included 4 sexually intact males, 13 castrated males, 6 sexually intact females, and 11 spayed females. The majority (n … 30) of study cats were domestic shorthair cats, and other breeds represented included Persian, Maine Coon, Siamese, and Turkish Van (1 each). Age of the cats ranged from 2 months to 10 years (mean ± SD, 33.9 ± 31.6 months). The height from which cats fell ranged from the second to the sixth floor (mean ± SD, 3.3 ± 1.1 floor). The number of days that cats were hospitalized ranged from 4 to 10 days (mean ± SD, 5.5 ± 1.8 days). On the basis of information obtained from the owners, none of the cats had a history of pancreatic disease before the fall.
Serum fPLI concentration—Nine of 34 (26.5%) cats had a serum fPLI concentration > 5.4 μg/L in at least 1 sample and were classified as having pancreatitis, whereas the remaining 25 cats (73.5%) were classified as not having pancreatitis. The mean serum fPLI concentrations for cats with and without pancreatitis at each blood collection time were summarized (Table 1). The mean serum fPLI concentrations determined for the initial physical examination and 24 hours after the initial physical examination were positively correlated (r … 0.552; P ≤ 0.001), as were those determined for the initial examination and 72 hours after the initial examination (r … 0.458; P … 0.007). Mean serum fPLI concentrations at initial examination and 24 hours after the initial examination were higher than those at 48 and 72 hours after initial examination. The overall mean serum fPLI concentration (4.35 μg/L) at initial examination was significantly higher than that at 48 (1.25 μg/L) and 72 (1.23 μg/L) hours after initial examination.
Mean (range) serum fPLI concentration during (within 12 hours after the fall) and at 24, 48, and 72 hours after the initial examination for cats with (serum fPLI concentration > 5.4 μg/L; n … 9) and without (serum fPLI concentration ≤ 5.4 μg/L; 25) traumatic pancreatitis subsequent to HRS that were examined at a veterinary teaching hospital between March 1 and October 31, 2009.
Serum fPLI concentration (μg/L) | ||||
---|---|---|---|---|
Time after initial examination (h) | ||||
Classification | Initial examination | 24 | 48 | 72 |
With pancreatitis | 11.14 (1.2–40.6) | 8.23 (0.9–57.7) | 2.05 (0.6–5.6)* | 1.77 (0.5–6.5)* |
Without pancreatitis | 1.52 (0.5–3.3) | 0.98 (0.5–2.1) | 0.92 (0.4–1.7) | 1.00 (0.6–2.2) |
All | 4.35 (0.5–40.6) | 3.11 (0.5–57.7) | 1.25 (0.4–5.6)* | 1.23 (0.5–6.5)* |
Within a classification group, value differs significantly (P < 0.05) from that at initial examination.
Abdominal ultrasonography—The most common abnormality detected in the cats during the first ultrasonographic examination was hypoechoic or heteroechoic pancreatic parenchyma (n … 21 cats), followed by an enlarged pancreas (13) and hyperechoic mesentery (3), and none of the cats had peritoneal effusion. The most common abnormality detected in the cats during the second ultrasonographic examination was an enlarged pancreas (n … 24 cats), followed by hypoechoic or heteroechoic pancreatic parenchyma (15), hyperechoic mesentery (7), and peritoneal effusion (3). Twenty-five of 34 (73.5%) cats had ≥ 1 ultrasonographic abnormality (ie, cumulative score > 0) associated with pancreatic trauma on at least 1 of the 2 examinations. On the basis of the results for the first abdominal ultrasonographic evaluation, only 1 of 34 (2.9%) cats had a cumulative score ≥ 3 and was classified as having traumatic pancreatitis, whereas 8 of 34 (23.5%) cats had a cumulative score ≥ 3 on the second ultrasonographic evaluation and were classified as having traumatic pancreatitis (Table 2). The proportion of cats with traumatic pancreatitis differed significantly (P … 0.007) between the first and second ultrasonographic examinations. Between the first and second ultrasonographic examinations, 7 cats had distinct changes in the appearance of the pancreas (Figure 1). The left pancreatic lobe in 3 cats and the right pancreatic lobe in 1 cat could not be detected during one of the ultrasonographic examinations; however, both the left and right pancreatic lobes were evaluated via ultrasonography at least once in all 34 cats.
Number of cats from Table 1 that received cumulative scores of 0, 1, 2, 3, and 4 on abdominal ultrasonography, which was performed twice (at 24 to 48 hours [first examination] and 72 to 96 hours [second examination] after the initial physical examination, with at least 48 hours between ultrasonographic examinations).
Examination | ||
---|---|---|
Cumulative score | First | Second |
0 | 13 | 10 |
1 | 8 | 8 |
2 | 12 | 8 |
3 | 1 | 7 |
4 | 0 | 1 |
During each ultrasonographic examination, the following abnormalities were evaluated: hypoechoic or heteroechoic pancreatic parenchyma, pancreatic enlargement, hyperechoic mesentery, and peritoneal effusion. For each examination, a cat was assigned 1 point for each abnormality present, and a cumulative score ≥ 3 was considered suggestive of traumatic pancreatitis.
See Table 1 for remainder of key.
Comparison of serum fPLI concentrations with abdominal ultrasonography for identification of cats with traumatic pancreatitis subsequent to HRS—Twelve of 34 (35%) cats with traumatic pancreatitis were identified on the basis of either a serum fPLI concentration > 5.4 μg/L (n … 9) or a cumulative score ≥ 3 on abdominal ultrasonography (8); 5 cats had both a serum fPLI concentration > 5.4 μg/L and a cumulative score ≥ 3 on abdominal ultrasonography. Thus, the extent of agreement between the 2 diagnostic methods for the diagnosis of traumatic pancreatitis was 79%, and the extent of agreement beyond chance (κ … 0.452) was significant (P < 0.01).
Clinical outcome—Three cats were euthanized prior to being discharged from the hospital; necropsy was performed on only one of these. Necropsy findings for that cat included multiple areas of hemorrhage and trauma in the spleen, liver, and thorax, whereas histologic evaluation of the pancreas was unremarkable; thus, pancreatitis was not the cause of that cat's clinical deterioration. That cat did not have a serum fPLI concentration > 5.4 μg/L; however, it did have a cumulative score of 4 on the second abdominal ultrasonographic examination. For the 2 cats that were euthanized but on which a necropsy was not performed, both had radiographic evidence of lung contusion, hemothorax, pneumothorax, and minimal ascites. Those 2 cats had cumulative scores of 2 and 3, respectively, on the second abdominal ultrasonographic examination, and 1 had a serum fPLI concentration > 5.4 μg/L. Results of the telephone interviews with the owners of the 31 cats that were discharged from the hospital revealed that none of the cats developed clinical signs (ie, anorexia and lethargy) of pancreatitis or were examined by their primary care veterinarian during the 2 to 3 weeks immediately after discharge.
Discussion
Results of the present study suggested that evaluation of serum fPLI concentration and repeated abdominal ultrasonography are clinically useful for the diagnosis of traumatic pancreatitis subsequent to HRS in cats. Investigators of several studies20,22,23,h have described the evaluation of serum fPLI concentration and abdominal ultrasonography as methods for the diagnosis of acute pancreatitis in cats; however, to our knowledge, the use of those methods to diagnose traumatic pancreatitis subsequent to HRS in cats had not been described prior to the present study. The pathological mechanism of traumatic pancreatitis in veterinary patients is unknown. In human patients, traumatic pancreatitis is believed to be caused by blunt trauma to the abdomen or subsequent compression of the pancreas, which results in pancreatic contusion, hemorrhage, partial laceration, or complete fracture.24,25
The prevalence (12/34 cats [35%]) of traumatic pancreatitis in the cats of the present study was higher than that reported by investigators of other studies4,11 and supported our supposition that traumatic pancreatitis subsequent to HRS in cats has historically been underdiagnosed. However, diagnosis of traumatic pancreatitis in the present study was made on the basis of a serum fPLI concentration > 5.4 μg/L or ≥ 3 abnormalities (ie, hypoechoic or heteroechoic pancreatic parenchyma, pancreatic enlargement, hyperechoic mesentery, and peritoneal effusion) detected during abdominal ultrasonography; traumatic pancreatitis could not be definitively confirmed because histologic results were not available for all study cats.
Results of the present study indicated that, in cats with traumatic pancreatitis subsequent to HRS, serum fPLI concentration increased within 12 hours after the fall, but decreased dramatically between 24 and 48 hours after the initial evaluation. Thus, evaluation of serum fPLI concentration in cats with HRS > 48 hours after the fall may be of limited to no value for detection of traumatic peritonitis. Cats in another studyh had increased serum fPLI concentrations for up to 10 days after pancreatitis was experimentally induced, which suggests that the mechanism by which serum fPLI concentration increased or was metabolized differs between cats with experimentally induced pancreatitis and those with traumatic pancreatitis. Additional research in a larger study population is necessary to elucidate the mechanism of fPLI production and metabolism in cats with traumatic pancreatitis, compared with that in cats with nontraumatic pancreatitis.
The criteria used by the radiologist to evaluate the ultrasonographic images of the cats of the present study were the same as those used in other studies20–22 that involved cats with acute pancreatitis to ensure standardized and impartial reporting of findings. During the first ultrasonographic examination that was conducted within 24 to 48 hours after the initial physical examination, 21 of the 34 study cats had at least 1 abnormality detected, the most common of which was hypoechoic or heteroechoic pancreatic parenchyma; however, none of the cats had peritoneal effusion. Subsequently, peritoneal effusion was detected in 3 cats during the second ultrasonographic examination that was conducted 48 hours after the first. These results differed from those of other studies,4,6,11 in which peritoneal effusion was commonly detected in cats with acute pancreatitis or pancreatic rupture subsequent to HRS. Serial ultrasonographic examinations have been recommended to maximize the sensitivity of ultrasonography for detection of pancreatitis.26 In human patients with abdominal trauma, a second abdominal ultrasonographic examination performed 24 hours after the initial examination increased the sensitivity of ultrasonography for detection of abdominal injury or peritoneal effusion from 31% to 72%.27 In the present study between the first and second ultrasonographic examinations, 7 cats developed additional abnormalities indicative of progressive pancreatitis, the most frequent of which were an enlarged pancreas and hyperechoic peripancreatic mesentery.
Evaluation of the pancreas of the cats of the present study may have been more thorough than that of cats in other studies,20,21 in which the pancreas was evaluated during a routine abdominal ultrasonographic procedure. In the present study, the fact that the sonographers who performed the examinations knew that the cats were being evaluated because of HRS may have biased them to examine the pancreatic region more intensely and interpret subtle findings differently than they would have had the cats being examined not had a history of HRS. Results of another study20 suggest that the indication of pancreatitis as a potential diagnostic rule-out on an ultrasonography request form is not associated with whether pancreatitis was subsequently diagnosed in a patient; however, these results should be interpreted with caution because of the small sample size (n … 20).
Presently, a definitive diagnosis of pancreatitis can only be made on the basis of histopathologic changes in the pancreas28; a diagnosis of pancreatitis is rarely possible solely on the basis of diagnostic imaging findings.23,26 For the cats of the present study, collection of a pancreatic biopsy specimen was not an inclusion criterion because it was unlikely that many owners would have consented to the procedure solely for the purpose of the study on account of the inadvisability of anesthetizing an already traumatized patient. Moreover, results of other studies16,29 indicate that histologic evaluation of pancreatic biopsy specimens is not always diagnostic when lesions are localized.
In the present study, 4 cats with a serum fPLI concentration > 5.4 μg/L had a cumulative score < 3 on both ultrasonographic examinations, and 2 cats with a cumulative score ≥ 3 on at least 1 ultrasonographic examination did not have a serum fPLI concentration > 5.4 μg/L. These results suggested that ultrasonography was not as sensitive as evaluation of serum fPLI concentration for detection of pancreatitis in cats and were similar to results of another study18 in which abdominal ultrasonography lacked sensitivity for diagnosing pancreatitis in cats unless it was used in combination with other diagnostic tests. It is also possible that abdominal abnormalities associated with traumatic pancreatitis may not become detectable ultrasonographically until > 4 days after injury, and all of the ultrasonographic examinations of the cats of the present study were performed ≤ 4 days after the injury. The ultrasonographic findings of the present study may also have been affected by the fact that multiple sonographers performed the examinations; effective ultrasonography is dependent on operator experience and scanning technique.22
On the basis of the criterion used to diagnose pancreatitis (serum fPLI concentration > 5.4 μg/L or ≥ 3 abnormalities present during abdominal ultrasonography) in the present study, 12 of 34 (35%) cats developed traumatic pancreatitis subsequent to HRS; however, the survival rate did not appear to differ between cats with and without traumatic pancreatitis. Results of a study29 that involved human patients with abdominal trauma suggest that isolated pancreatic injuries, even a complete transection of the pancreas, can remain undiagnosed and heal spontaneously. The phenomenon of spontaneous pancreatic healing may provide an explanation for the clinical outcome of 9 cats in the present study that each had a serum fPLI concentration > 5.4 μg/L but no other clinical signs of pancreatitis during or within the 2 to 3 weeks after hospitalization. Regardless, the results of the present study suggested that diagnosis of traumatic pancreatitis subsequent to HRS in cats is difficult.
Results of the present study indicated that evaluation of serum fPLI concentration in combination with repeated abdominal ultrasonographic examinations may be clinically useful for the noninvasive diagnosis of traumatic pancreatitis subsequent to HRS in cats, especially in those cats that are subclinically affected. However, serum fPL concentration appears to be increased only transiently (ie, < 48 hours) in affected cats. Because of the strict inclusion criteria for the present study, the number of cats evaluated because of HRS was relatively small (n … 34). Additional studies that involve a larger population of cats with HRS are warranted to critically evaluate the prognostic usefulness of evaluation of serum fPLI concentration in combination with abdominal ultrasonography for the diagnosis of traumatic pancreatitis.
ABBREVIATIONS
CI | Confidence interval |
fPLI | Feline-specific pancreatic lipase immunoreactivity |
HRS | High-rise syndrome |
Dupre G, Allenou A, Bouvy B. High-rise syndrome: a retrospective study on 413 cats (abstr). Vet Surg 1995;24:294.
Forman MA, Shiroma J, Armstrong PJ, et al. Evaluation of feline pancreas-specific lipase (Spec fPL) for the diagnosis of feline pancreatitis (abstr). J Vet Intern Med 2009;23:733–734.
Texas A&M Gastrointestinal Laboratory, College Station, Tex.
Spec fPL Test, IDEXX Reference Laboratories, Westbrook, Me.
HDI 5000, Philips, Amsterdam, The Netherlands.
HDI 5000 Sono CT, Philips, Amsterdam, The Netherlands.
SPSS, version 17.0, SPSS Inc, Chicago, Ill.
Williams DA, Steiner JM, Ruaux CG, et al. Increases in serum pancreatic lipase immunoreactivity (PLI) are greater and of longer duration than those of trypsin-like immunoreactivity (TLI) in cats with experimental pancreatitis (abstr). J Vet Intern Med 2003;17:445.
References
1. Robinson BW. The high rise trauma syndrome in cats. Feline Pract 1976; 6(5):40–43.
2. Diamond JM. Why cats have nine lives. Nature 1988; 332: 586–587.
3. Whitney WO, Melhaff CJ. High-rise syndrome in cats (Erratum published in J Am Vet Med Assoc 1988; 192:542). J Am Vet Med Assoc 1987; 191: 1399–1403.
4. Lettow E, Kabisch D, Arnold U. Pankreasruptur nach Fenstersturz bei der Katze. Kleintierpraxis 1986; 31: 161–212.
5. Barth R. Die polytraumatisierte Katze. Kleintierpraxis 1990; 35: 321–330.
6. Westermarck E, Saario E. Traumatic pancreatic injury in a cat—a case history. Acta Vet Scand 1989; 30: 359–362.
7. Kapatkin AS, Matthiesen DT. Feline high-rise syndrome. Compend Contin Educ Pract Vet 1991; 13: 1389–1394.
8. Vnuk D, Pirkic B, Maticic D, et al. Feline high-rise syndrome: 119 cases (1998–2001). J Feline Med Surg 2004; 6: 305–312.
9. Papazoglou LG, Galatos AD, Patsikas MN, et al. High-rise syndrome in cats: 207 cases (1988–1998). Aust Vet Pract 2001; 31: 98–102.
10. Flagstad A, Arnbjerg J, Jensen SE. Feline high-rise syndrome in the greater metropolitan area of Copenhagen. A four-year retrospective study. Eur J Comp Anim Pract 1998; 9: 165–171.
11. Liehmann LM, Dörner J, Hittmair KM, et al. Pancreatic rupture in four cats with high-rise syndrome. J Feline Med Surg 2012; 14: 131–137.
12. Suter PF, Olsson SE. Traumatic hemorrhagic pancreatitis in the cat: a report with emphasis on the radiological diagnosis. J Am Vet Radiol Soc 1969; 10: 4–11.
13. Crane SW. Evaluation and management of abdominal trauma in the dog and cat. Vet Clin North Am Small Anim Pract 1980; 10: 655–689.
14. Hill RC, Van Winkle TJ. Acute necrotizing pancreatitis and acute suppurative pancreatitis in the cat: a retrospective study of 40 cases (1976–1989). J Vet Intern Med 1993; 7: 25–33.
15. Kitchell BE, Strombeck DR, Cullen J, et al. Clinical and pathologic changes in experimentally induced acute pancreatitis in cats. Am J Vet Res 1986; 47: 1170–1173.
16. De Cock HEV, Forman MA, Farver TB, et al. Prevalence and histopathology characteristics of pancreatitis in cats. Vet Pathol 2007; 44: 39–49.
17. Ragozzino A, Manfredi R, Scaglione M, et al. The use of MRCP in the detection of pancreatic injuries after blunt trauma. Emerg Radiol 2003; 10: 14–18.
18. Zoran DL. Pancreatitis in cats: diagnosis and management of a challenging disease. J Am Anim Hosp Assoc 2006; 42: 1–9.
19. Steiner JM, Wilson BG, Williams DA. Development and analytical validation of a radioimmunoassay for the measurement of feline pancreatic lipase immunoreactivity in serum. Can J Vet Res 2004; 68: 309–314.
20. Saunders HM, VanWinkle TJ, Drobatz K, et al. Ultrasonographic findings in cats with clinical, gross pathologic, and histologic evidence of acute pancreatic necrosis: 20 cases (1994–2001). J Am Vet Med Assoc 2002; 221: 1724–1730.
21. Ferreri JA, Hardam E, Kimmel SE, et al. Clinical differentiation of acute necrotizing from chronic nonsuppurative pancreatitis in cats: 63 cases (1996–2001). J Am Vet Med Assoc 2003; 223: 469–474.
22. Forman MA, Marks SL, De Cock HEV, et al. Evaluation of serum feline pancreatic lipase immunoreactivity (fPLI) and helical computed tomography versus conventional testing for the diagnosis of feline pancreatitis. J Vet Intern Med 2004; 18: 807–815.
23. Gerhardt A, Steiner JM, Williams DA, et al. Comparison of the sensitivity of different diagnostic tests for pancreatitis in cats. J Vet Intern Med 2001; 15: 329–333.
24. Teh SH, Sheppard BC, Mullins RJ, et al. Diagnosis and management of blunt pancreatic ductal injury in the era of high-resolution computed axial tomography. Am J Surg 2007; 193: 641–643.
25. Gupta A, Stuhlfaut JW, Fleming KW, et al. Blunt trauma of the pancreas and biliary tract: a multimodality imaging approach to diagnosis. Radiographics 2004; 24: 1381–1395.
26. Hecht S, Henry G. Sonographic evaluation of the normal and abnormal pancreas. Clin Tech Small Anim Pract 2007; 22: 115–121.
27. Blackbourne LH, Soffer D, McKenney M, et al. Secondary ultrasound examination increases the sensitivity of the FAST exam in blunt trauma. J Trauma 2004; 57: 934–938.
28. Steiner JM. Diagnosis of pancreatitis. Vet Clin North Am Small Anim Pract 2003; 33: 1181–1195.
29. Leppäniemi A, Haapiainen R, Kiviluoto T, et al. Pancreatic trauma: acute and late manifestations. Br J Surg 1988; 75: 165–167.