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).
Feline-specific pancreatic lipase immunoreactivity
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.
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.
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.
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.
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.
29. Leppäniemi A, Haapiainen R, Kiviluoto T, et al. Pancreatic trauma: acute and late manifestations. Br J Surg 1988; 75: 165–167.