Comparison of ultrasonographic echogenicity and outcome in cats with suspected pancreatitis

Abstract

Objectives

The aim of this study was to determine whether ultrasonographic pancreatic echogenicity, especially hypoechogenicity, has an impact on the prognosis of cats with suspected pancreatitis. We hypothesised that cats with a hypoechoic pancreas have a longer duration of hospitalisation, higher treatment costs and a higher mortality rate.

Methods

This was a retrospective study, which included cats with clinical signs of pancreatitis, a SNAP fPL test result above the reference interval and ultrasonographic abnormalities consistent with pancreatitis. Medical records and follow-up information were retrieved from the local electronic database. Cases were assigned to one of three groups based on pancreatic echogenicity: hypoechoic, hyperechoic or mixed echogenicity. Statistical analysis aimed to assess differences in outcome, ultrasonographic abnormalities, historical features, physical examination findings, laboratory results, concurrent diseases or treatment costs.

Results

Thirty-six (64%) cats with a hypoechoic, seven (13%) with a hyperechoic and 13 (23%) cats with a mixed echoic pancreas were included. Cats with a hypoechoic pancreas had a significantly lower median body weight (P = 0.010) and lower median body condition score (P = 0.004) compared with the other cats. Furthermore, they were presented as being lethargic significantly more often (P = 0.014), were more likely to have a homogeneously enlarged pancreas (P <0.001) and were less likely to have concurrent abnormalities or diseases, such as ultrasonographic enteric abnormalities (P = 0.020), triaditis (P = 0.013) and diabetes mellitus (P = 0.041). However, there was no difference in treatment costs (P = 0.961), duration of hospitalisation (P = 0.898), survival of hospitalisation (P = 0.419) or survival time (P = 0.256) between groups.

Conclusions and relevance

In this study, echogenicity was of no prognostic value in cats with suspected pancreatitis. Cats with a hypoechoic pancreas were not associated with a poorer outcome than cats with a hyperechoic or mixed echoic pancreas.

Keywords

Hypoechoic pancreas ultrasound pancreatitis pancreatic prognosis

Introduction

Histologically, feline pancreatitis can be divided into acute and chronic disease.^1,2 In chronic pancreatitis, fibrosis, acinar atrophy and mild-to-moderate lymphocyte infiltration are the predominant features, whereas acute pancreatitis is characterised by necrosis of acinar cells, neutrophilic inflammation associated with interstitial oedema and peripancreatic fat necrosis.^1,2 Irrespective of its classification, history and physical examination findings are often non-specific, and severity of the disease may vary from asymptomatic to severe.^2,3

The prognosis is considered to be dependent on the severity, as well as duration of the disease, amount of pancreatic necrosis, the presence of systemic complications (eg, disseminated intravascular coagulation, pulmonary thromboembolism and multiorgan failure) and concurrent disorders.^1,4–6 In human medicine, patients with pancreatic necrosis have been shown to have a higher mortality rate than patients without necrosis, and, in dogs, pancreatic necrosis is associated with longer hospitalisation and more relapses.^7,8

In ultrasonography, the normal feline pancreatic echotexture is homogeneous and the echogenicity is nearly isoechoic to the surrounding mesenteric fat, isoechoic or slightly hyperechoic to the liver and hypoechoic to the spleen.⁹ The pancreatic duct is visible in the centre of the pancreatic parenchyma as an anechoic, tubular structure with a surrounding thin hyperechoic wall.⁹ The thickness of the pancreas ranges from 0.5 to 0.9 cm in the left lobe and the pancreatic body, and from 0.3 to 0.6 cm in the right lobe.¹⁰

The most common ultrasonographic findings in feline pancreatitis are an increased echogenicity of the mesenteric fat bordering the pancreas, peritoneal effusion, increase in pancreatic thickness, irregular pancreatic margins, hypoechoic or hyperechoic appearance, mixed echogenicity and pancreatic masses/cysts.^11–13 The peripancreatic hyperechogenicity is consistent with peripancreatic steatitis and saponification of fat.¹⁴ Decreased echogenicity in acute pancreatitis is thought to be a result of oedema, inflammatory infiltrate and necrosis. In contrast, increased echogenicity suggests fibrotic changes.^15,16

The primary objective of this study was to determine whether ultrasonographic pancreatic echogenicity can be used as a prognostic marker of disease severity. As a hypoechoic pancreas indicates necrosis, at least to some degree, our hypothesis was that cats with a hypoechoic pancreas would have a poorer outcome (longer duration of hospitalisation, higher treatment costs and a higher mortality rate).

Materials and methods

The database of the University of Veterinary Medicine Vienna was searched for cats suspected of having pancreatitis based on abdominal ultrasound findings between July 2011 and May 2017, with pancreatic echogenicity described as either hypoechoic, hyperechoic or mixed. The ultrasonographic diagnosis of suspected pancreatitis was made based on the presence of any of the following: hyperechoic peripancreatic fat, peritoneal effusion, increase in pancreatic thickness, irregular pancreatic margins and change in echogenicity.

Cases with a SNAP fPL test (IDEXX) above the reference interval (>3.5 μg/l) were included. Each patient’s medical records were reviewed and cases with at least two historical features or physical examination findings consistent with pancreatitis were included. Historical features compatible with pancreatitis were determined as lethargy, vomiting, anorexia, diarrhoea and/or weight loss. Physical examination findings consistent with pancreatitis were hypothermia, hyperthermia, dehydration, icterus, pale mucous membranes and/or a painful abdomen.

As many cats with pancreatitis have concomitant diseases such as hepatic lipidosis, cholangitis, inflammatory bowel disease (IBD), triaditis and diabetes mellitus,^3,17 and hyperthyroidism and chronic kidney disease are common in older cats,¹⁸ cats with uncomplicated diabetes mellitus, mildly elevated creatinine concentrations (International Renal Interest Society [IRIS] stage ⩽2), as well as hyperthyroidism, IBD, suspected and confirmed hepatobiliary disease, or suspected triaditis were included. Cats without hospitalisation, asymptomatic patients, patients with previous surgery, a history of trauma, neoplasia or concurrent severe systemic diseases (eg, feline infectious peritonitis, diabetic ketoacidosis and IRIS stage ⩾3 renal failure) were excluded.

All ultrasound examinations were performed in right lateral recumbency by a single radiologist with over 25 years of experience in the field of ultrasonography. An 8–5 MHz curved array transducer and/or a 12–5 MHz linear array transducer (HDI 5000 and iU22; Philips) were used.

Included cats were assigned to one of three groups. Group A included all cats with an ultrasonographic hypoechoic pancreas compared with the surrounding fatty tissue, the liver and the spleen. In the case of hyperechoic peripancreatic fat, only the liver and spleen were used for echogenicity comparison. Group B included all cats with a hyperechoic pancreas compared with the surrounding fat, liver and spleen. Cats with mixed echogenicity were assigned to group C. Mixed echogenicity was defined as an echo intensity (brightness) ranging from hypoechoic to hyperechoic. Cases were included if the pancreas had patchy hypoechoic and hyperechoic areas throughout the parenchyma (in this example, the echotexture was termed ‘heterogeneous’); they were also included if a portion of the pancreas had a different echogenicity than the rest of the pancreas and when the pancreas had a normal echogenicity but other signs consistent with pancreatitis (Figures 1 and 2).

Figure 1

Ultrasound images of a (a) hypoechoic, (b) hyperechoic and (c) mixed echoic pancreas. Pancreases are between the measuring calipers in all images. (a) The hypoechoic pancreas being measured between the calipers (14 mm) has a homogeneous parenchyma and irregular margins; note the increased echogenicity of the mesenteric fat bordering the pancreas. In (b), the left lobe of the pancreas is diffusely hyperechoic compared with the surrounding fat; the pancreatic duct is visible as an anechoic tubular structure running through the pancreatic parenchyma. The left pancreatic lobe in image (c) has a mixed echogenicity; it is partially isoechoic to the mesenteric fat bordering the pancreas and has multifocal areas of increased echogenicity, resulting in a heterogeneous parenchymal texture

Figure 2

Ultrasound images of the pancreas (between the measuring calipers) of a (a) group A, (b) group B and (c) group C cat obtained with a (a,c) micro-convex and (b) linear array probe, respectively. Comparison of echogenicity to parenchyma of the liver and spleen: (a) the pancreas is hypoechoic to the spleen (*) with hyperechoic fat surrounding the pancreas; (b) hyperechoic pancreas in comparison to the spleen (*); and (c) the pancreas is isoechoic to slightly hyperechoic to the liver (**), is enlarged (13.5 mm thickness), has irregular margination and hyperechoic peripancreatic fat is evident

Parameters used to characterise disease severity and outcome were duration of hospitalisation, survival of hospitalisation, survival time, time from admittance to voluntary intake of food, recurrence, time to recurrence and treatment costs. Recurrence was diagnosed if the cats re-presented with clinical signs consistent with pancreatitis and a SNAP fPL test result above the reference interval within 3 weeks and up to 4 years after hospital discharge. Time to recurrence was measured from the day of discharge to the day of re-presentation at the clinic. Owners were contacted by telephone to obtain follow-up information, if it was not documented in the local electronic database.

Sex, breed, age, body condition score (BCS), weight and duration of clinical signs prior to presentation were recorded. Patient assessment also included historical features (lethargy, vomiting, anorexia, diarrhoea, weight loss); results of the physical examination (hypothermia, hyperthermia, dehydration, icterus, pale mucous membranes, painful abdomen); serum biochemistry and electrolytes when available (lipase, alanine transaminase [ALT], gamma-glutamyl transpeptidase, glutamate dehydrogenase, alkaline phosphatase, total bilirubin, glucose, calcium and potassium); haematocrit, erythrocytes and leukocytes; concurrent diseases (diabetes mellitus, hyperthyroidism, IBD, suspected or confirmed hepatobiliary disease and triaditis); and ultrasonographic findings (enlarged pancreas, heterogeneous parenchymal texture, hyperechoic peripancreatic fat, peritoneal effusion, pancreatic nodules/cysts, enlarged lymph nodes, hepatic abnormalities, dilated common bile duct, gallbladder abnormalities and enteric abnormalities). Enlargement of the pancreas was defined as measuring >1 cm in diameter at the pancreatic body and/or left lobe.¹⁰ Lymph nodes were measured according to previously published literature.¹⁹ Ultrasonographic hepatic abnormalities were defined as changes in echogenicity or echotexture or increase in size. The common bile duct was defined as dilated if >4 mm in diameter.²⁰ Gallbladder abnormalities were noted as wall thickness >1 mm and/or the presence of sludge.²¹ An increase in intestinal mucosal layer echogenicity and thickening of the muscularis propria (when the width of the muscular layer was greater than half the thickness of the submucosal layer) were summarised as ultrasonographic enteric abnormalities.²²

A BCS from 1 (emaciated) to 5 (obese) was applied.²³ Hyperthermia and hypothermia were defined as a body temperature >39.3°C and <38.0°C, respectively.²⁴ A diagnosis of diabetes mellitus was made when blood glucose concentrations exceeded the renal threshold (230–290 mg/dl) and fructosamine concentrations were above the upper limit of the reference interval (400 mol/l).^25–27 A thyroxine concentration >48 nmol/l was considered diagnostic of hyperthyroidism.²⁸ Histological diagnosis of IBD was determined via full-thickness biopsy. Suspected hepatobiliary disease was defined as the presence of ultrasonographic abnormalities of the liver and/or the gallbladder in combination with elevated bilirubin and/or ALT levels. Hepatobiliary disease was confirmed by cytological or bacteriological examination of specimens obtained by ultrasound-guided fine-needle aspiration (FNA) of the liver and/or cholecystocentesis. Triaditis was suspected when cats had serum biochemistry and ultrasonographic changes consistent with inflammation of the hepatobiliary system, pancreas and small intestine.

Statistical analysis

IBM SPSS Statistics 24 was used for the analyses. Metric data (eg, age, weight, survival time and duration of hospitalisation) were tested for normality using the Kolmogorov–Smirnov test. Comparison between groups was performed using Kruskal–Wallis and Dunn’s post-hoc test. Categorical variables (eg, historical features, physical examination, ultrasonographic abnormalities and concurrent disease) were compared using contingency tables and Fisher’s exact test. Survival data were examined by Kaplan–Meier survival analysis and the log-rank test. Associations between variables were tested in a pairwise fashion using the Spearman’s rank order correlation coefficient. Results were considered statistically signiﬁcant if P ⩽0.05.

Results

Study population

Fifty-six cats met the inclusion criteria. Thirty-six (64%) cats were assigned to group A, seven (13%) to group B, and 13 (23%) to group C.

There were 29 (52%) neutered males, one (2%) intact male, 23 (41%) spayed females and three (5%) intact females in the study. Differences in sex distribution identified between groups were not significant (P = 0.165). Breeds included domestic shorthair (n = 46), domestic longhair (n = 2), Maine Coon (n = 2), Burmese (n = 1), Birman (n = 1), Maine Coon mixed breed (n = 1), Siamese (n = 1), Persian (n = 1) and Norwegian Forest Cat (n = 1).

Median (range) age, BCS, weight and duration of clinical signs are provided in Table 1. The median body weight of cats in group A was significantly lower compared with those in group B (P = 0.018) and group C (P = 0.045). Median BCS was significantly lower in cats in group A than in cats in group B (P = 0.006), with no difference between cats in group A and group C (P = 0.091).

Table 1

Age, body condition score (BCS), weight and duration of clinical signs

	Group A	Group B	Group C	P
Age (months)	163 (32–219)	127 (67–174)	129 (57–180)	0.227
Body condition score	2 (1–5)	4 (3–5)	3 (1–5)	0.004
Weight (kg)	4.00 (2.26–5.81)	5.22 (4.15–6.11)	4.85 (2.5–7.6)	0.010
Duration of clinical signs (days)	4.00 (0.1–210)	4.00 (2–60)	6.00 (0.6–144)	0.715

Data are median (range)

Group A = hypoechoic pancreas; group B = hyperechoic pancreas; group C = mixed echogenicity

There were no significant differences in clinical pathology results or therapy between groups (see Table 1 in the supplementary material).

Historical features and physical examination

Owing to some missing data, groups B and C were combined for comparison of history and physical examination findings, which are summarised in Table 2. Results of the individual groups can be found in Table 2 in the supplementary material. Lethargy was the only finding that differed significantly between groups (P = 0.014).

Table 2

History and physical examination findings

	Group A (n = 36)	Group B + C (n = 20)	P value
Lethargy	27/34 (79)	8/19 (42)	0.014
Vomiting	28/35 (80)	15/20 (75)	0.740
Anorexia	32/36 (89)	14/20 (70)	0.084
Diarrhoea	17/34 (50)	11/20 (55)	0.783
Weight loss	14/25 (56)	6/12 (50)	1.000
Hypothermia	6/34 (18)	2/18 (11)	0.698
Hyperthermia	5/34 (15)	2/18 (11)	1.000
Dehydration	32/36 (89)	15/20 (75)	0.256
Icterus	5/36 (14)	4/20 (20)	0.707
Pale mucous membranes	2/36 (5)	0/20 (0)	0.532
Painful abdomen	16/36 (44)	9/20 (45)	1.000

Data are n (%)

Group A = hypoechoic pancreas; group B = hyperechoic pancreas; group C = mixed echogenicity

Ultrasonographic findings

Ultrasonographic abnormalities are given in Table 3. The most consistent finding was enlargement of the pancreas, identified in 84% of all cases. Cats in group A were significantly more likely to have an enlarged pancreas (P <0.001) with homogeneous parenchyma (P = 0.012) than the other two groups. Cats in group C were associated with ultrasonographic enteric abnormalities (P = 0.020).

Table 3

Ultrasonography findings

	Group A (n = 36)	Group B (n = 7)	Group C (n = 13)	P value
Heterogeneous parenchymal texture	9 (25)	5 (71)	8 (62)	0.012
Enlarged pancreas	35 (97)	3 (43)	9 (69)	<0.001
Hyperechoic peripancreatic fat	8 (22)	0 (0)	4 (31)	0.317
Peritoneal effusion	6 (17)	3 (43)	4 (31)	0.207
Pancreatic nodules/cysts	3 (8)	0 (0)	1 (8)	1.000
Enlarged lymph nodes	13 (36)	2 (29)	9/12 (75)	0.052
Hepatic abnormalities	20 (56)	4 (57)	6 (46)	0.922
Dilated common bile duct	12 (33)	2 (29)	3 (23)	0.908
Gallbladder abnormalities	16 (44)	1 (14)	5 (38)	0.338
Enteric abnormalities	16 (44)	2 (29)	11 (85)	0.020

Data are n (%)

Group A = hypoechoic pancreas; group B = hyperechoic pancreas; group C = mixed echogenicity

Concurrent diseases

The frequency of concurrent diseases is summarised in Table 4. Ultrasonographic abnormalities of the small intestine (P = 0.020) and suspected triaditis (P = 0.013) occurred more frequently in cats in group C than in cats in the other two groups. There was no difference in the frequency of ultrasonographic hepatobiliary abnormalities, or suspected or confirmed hepatobiliary disease. In the eight cases in which hepatobiliary disease was confirmed, FNA cytology revealed cholangitis, cholecystitis and hepatic lipidosis. Bacteria were cultured from the gallbladder in one cat and from the liver in another. When groups B and C were considered together, significantly more cats in those two groups had concurrent diabetes mellitus compared with cats in group A (P = 0.041). Only four cats in the entire study population had no additional ultrasonographic abnormalities other than those suggestive of pancreatitis and were free of suspected concurrent disease.

Table 4

Occurrence of concurrent diseases

	Group A (n = 36)	Group B (n = 7)	Group C (n = 13)	P value
Diabetes mellitus	4 (11)	3 (43)	4/ (31)	0.058
Hyperthyroidism	5 (14)	1 (14)	1 (8)	1.000
US enteric abnormalities	16 (44)	2 (29)	11 (85)	0.020
Confirmed IBD	3 (8)	0 (0)	1 (8)	1.000
US hepatobiliary abnormalities	28 (78)	4 (57)	9 (69)	0.446
Suspected hepatobiliary disease	17 (47)	4 (57)	5 (38)	0.729
Confirmed hepatobiliary disease	4 (11)	2 (29)	2 (15)	0.316
Suspected triaditis	5 (14)	2 (29)	7 (54)	0.013
Absent concurrent disease	2 (6)	1 (14)	1 (8)	0.587

Data are n (%)

Group A = hypoechoic pancreas; group B = hyperechoic pancreas; group C = mixed echogenicity; US enteric abnormalities = ultrasonographic abnormalities of the small intestine; confirmed IBD = histological diagnosis of inflammatory bowel disease (IBD) determined via full-thickness biopsy; US hepatobiliary abnormalities = ultrasonographic abnormalities of the liver and/or the gallbladder; suspected hepatobiliary disease = ultrasonographic abnormalities of the liver and/or the gallbladder in combination with elevated bilirubin and/or alanine transaminase (ALT) levels; confirmed hepatobiliary disease = cytological or bacteriological confirmation of hepatobiliary disease by ultrasound-guided hepatic fine-needle aspiration and/or cholecystocentesis; suspected triaditis = ultrasonographic abnormalities of the hepatobiliary system, small intestine and the pancreas as well as elevated bilirubin and/or ALT levels

Outcome

Duration of hospitalisation, survival, survival time after discharge, time from admittance to voluntary intake of food, recurrence and the time to recurrence did not differ between groups (Table 5).

Table 5

Outcome parameters

	Group A (n = 36)	Group B (n = 7)	Group C (n = 13)	P value
Survival of hospitalisation	30 (83)	5 (71)	12 (92)	0.419
Recurrence	9 (25)	1 (14)	5 (38)	0.523
Survival time (days)	603 (63–1855)	691 (210–1030)	1000 (30–1670)	0.256
Duration of hospitalisation (days)	5 (1–19)	5 (3–21)	6 (2–10)	0.898
Time from admittance to voluntary intake of food (days)	3 (0–15)	1 (0–6)	3 (0–15)	0.433
Time to recurrence (days)	291 (63–970)	553	195 (21–1606)	0.686
Treatment costs (€)	790.42 (271.08–2370.61)	851.95 (493.83–2357.20)	815.07 (439.42–1809.74)	0.961

Survival of hospitalisation and recurrence data are n (%); all other data are median (range)

P values are given for comparison of outcome variables between groups

Group A = hypoechoic pancreas; group B = hyperechoic pancreas; group C = mixed echogenicity

Thirty of 36 cats in group A, 5/7 cats in group B and 12/13 cats in group C survived hospitalisation. No significant difference was detected for survival times between groups (Figure 3). There was no correlation between survival times and duration of hospitalisation (P = 0.636), or between survival times and time from admittance to voluntary intake of food (P = 0.216).

Figure 3

Kaplan–Meier survival curves. Vertical marks represent censored cats. The x-axis shows survival time in days since discharge and the y-axis the proportion surviving.

As cats in group C had significantly more frequent ultrasonographic enteric abnormalities and suspected triaditis, and diabetes mellitus was detected more frequently in groups B and C, these parameters were compared to survival of hospitalisation, independently of group. There was no significant difference in mortality for the presence of ultrasonographic enteric abnormalities (P = 0.288), triaditis (P = 0.676) and diabetes mellitus (P = 0.671).

Discussion

Acute and chronic feline pancreatitis can vary from mild to severe and show overlapping ultrasonographic abnormalities.^1,2,10,29,30 Based on the assumption that a hypoechoic pancreas represents, at least to some extent, necrosis, we hypothesised that this specific pancreatic appearance is associated with a poorer outcome and can be used as a prognostic marker. The results of this study provide evidence against the proposed hypothesis. There was no difference in outcome between cats with either hypoechoic, hyperechoic or mixed echoic parenchyma.

Necrosis is present in 96% of dogs with fatal acute pancreatitis.³¹ In an experimental study on five Beagle dogs, necrosis was demonstrated by Maier³² to be hypoechoic, where cases with 75–100% necrosis of the pancreas on microscopy were hypoechoic on ultrasound. Conversely, ultrasonography of the pancreas was normal in most cases of minimal necrosis (⩽25%).³²

As necrosis cannot be distinguished from oedema in B-mode ultrasonography,³³ we speculate that the homogeneously enlarged hypoechoic pancreas on ultrasound in this study could have, in fact, represented oedema. The typical ultrasonographic sign for pancreatic oedema in dogs is the so-called ‘tiger-stripe’ pattern, which represents poorly circumscribed hypoechoic foci to well-defined linear anechoic fissures and subcapsular anechoic spaces.³⁴ In human medicine, an enlarged diffusely hypoechoic pancreas is consistent with oedematous pancreatitis on endoscopic ultrasound, whereas in necrotising pancreatitis, the gland is also enlarged but tends to show a heterogeneous parenchymal texture with hypoechoic circumscribed areas.³⁵ In our study, a hypoechoic pancreas was associated with enlargement and homogeneous parenchyma in most cases, and thus would also fit the description of oedematous pancreatitis in human medicine.³⁵

In people, the gold standard method to distinguish necrosis from oedema is CT with intravenous contrast administration; in oedematous pancreatitis the gland enhances homogeneously, whereas necrosed areas do not enhance.³⁶ This has clinical relevance as necrosis is associated with a higher mortality rate.⁷ In dogs, heterogeneous contrast enhancement of the pancreas in CT is consistent with necrotic areas and associated with a longer duration of hospitalisation, more relapses and a higher frequency of portal vein thrombosis.^8,37 Limited availability and the need of anaesthesia, but most of all the very low sensitivity for diagnosing feline pancreatitis, inhibits the use of CT in feline practice.^38,39 A previous study with MRI showed promising results in the detection of feline pancreatitis, but there have not been any studies correlating the results with necrosis or patient outcome.⁴⁰ Using contrast-enhanced Doppler ultrasonography, Rademacher et al⁴¹ identified a difference in vascularity and blood volume in healthy cats and cats with pancreatic disorders. However, to our knowledge, there is no literature correlating contrast-enhanced ultrasonography (CEUS) results with feline patient outcome. In people and dogs, CEUS can distinguish necrosis from interstitial pancreatitis.^42–44 Studies in cats are strongly encouraged.

In the current study, body weight and BCS were lower in cats with a hypoechoic pancreas than either hyperechoic or mixed echoic pancreas. Weight loss is a common complaint in cats with pancreatitis; thus, it could be concluded that these cats had a longer duration of disease. The results of this study contradict this explanation. It is possible that cats with a hypoechoic pancreas had a lower initial weight. Conversely, cats with a higher BCS could have an increase in echogenicity of the pancreas owing to fatty infiltration. In people, such an increase in pancreatic echogenicity is described as a result of an increase in age and body weight.^45–47 The terminology fatty pancreas, pancreatic lipomatosis or steatosis is used, and has also been described in a single case report in a dog.^48–50 A hyperechoic pancreas also correlated with dogs having hyperadrenocorticism.⁵¹ In clinically healthy cats, there was no increase in echogenicity with age;⁵² however, no studies have investigated the relationship of body fat and echogenicity of the feline pancreas.

Although feline pancreatitis is associated with many different concurrent diseases,^{1,3,5,13,14,29,53} their impact on patient outcome is uncertain. Similar to previous studies, more than half of the cats in this study had confirmed concurrent disorders and 93% had at least suspected concurrent disease.^13,53 This is comparable to a study in which 92% of cats were found to have concomitant disorders.³ In this study, 54% of the cats had ultrasonographic hepatic abnormalities, 39% had gallbladder abnormalities and 30% had a dilated common bile duct. Group differences were not observed. As a normal liver size, echogenicity and normal biliary system on ultrasound does not exclude feline cholangitis, these results should be interpreted with caution.⁵⁴ Interestingly, cats with a hypoechoic pancreas were statistically less likely to have concurrent diseases, such as ultrasonographic enteric abnormalities, triaditis and diabetes mellitus. Although it is possible that this improved the outcome in cats with this specific pattern, cats with diabetes mellitus or the suspicion of triaditis did not have a poorer outcome in this study.

Of note, cats with a hypoechoic pancreas tended to be more lethargic than cats with hyperechoic or mixed echoic pancreas. An association with pain seems possible. Lethargy, as well as decreased appetite or decreased grooming, can be a sign of pain.⁵⁵ In dogs, a painful abdomen is a common finding on physical examination.³¹ In people, acute and chronic pancreatitis are also characterised by persistent and severe pain.⁵⁶ This is caused by fibrosis, ischaemia, recurrent acute inflammation with necrosis of the pancreas or increased pancreatic pressure, which also has been demonstrated in an experimental study with cats.^57–61

This study had several limitations. The first was the small sample size, particularly in groups B and C. This was mainly due to the retrospective nature of the study design and the strict exclusion criteria. The small number of cases weakened the statistical analyses and conducting a power analysis would have been ideal. A further limitation of this retrospective study was that it was not possible to determine the actual number of cats with concurrent diseases because histopathology is required for diagnosis. For this reason, we included the parameters with suspected concomitant disorders, which is probably closer to the actual number. However, it was not possible to determine the severity of these concomitant diseases. Another limitation was the lack of histopathology, which, again, was based on the retrospective study design. FNA or biopsy of the pancreas were only performed in four cats, and only three cats underwent necropsy. Histopathology of incisional pancreatic biopsies is currently considered the gold standard for ante-mortem diagnosis of feline pancreatitis.^2,3,62 However, because of the frequently multifocal nature with lesions scattered throughout the pancreas, a single biopsy may be insufficient to exclude pancreatitis.^2,62–64 Based on necropsy examinations, chronic pancreatitis is also evident in clinically sound cats and, therefore, the clinical significance of histopathologically mild pancreatitis is debatable.³⁸ In addition, cats with severe pancreatitis are often not suitable candidates for anaesthesia.^62,64

Although a SNAP fPL test was performed in all patients, Spec fPL or 1,2-o-dilauryl-rac-glycero-3-glutaric acid ± (6′-methylresorufin) ester (DGGR) lipase measurements to further support a diagnosis of pancreatitis were performed in only a small number of these cats. Of note, the primary aim of this study was not to diagnose feline pancreatitis, but to investigate whether pancreatic echogenicity, especially hypoechogenicity, has an impact on the prognosis in cats with ‘suspected’ pancreatitis.

Conclusions

Echogenicity was of no prognostic value in cats with suspected pancreatitis in this study. Cats with an ultrasonographically hypoechoic pancreas were not associated with a poorer outcome than cats with a hyperechoic or mixed echoic pancreas. Studies are encouraged to investigate whether this specific ultrasonographic appearance actually represents oedematous pancreatitis rather than necrosis in cats.

Supplemental Material

Table 1

Clinical pathology results

Supplemental Material

Table 2

History and physical examination findings

Footnotes

Accepted: 30 December 2021

Conflict of interest

The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding

The authors received no financial support for the research, authorship, and/or publication of this article.

Ethical approval

The work described in this manuscript involved the use of non-experimental (owned or unowned) animals. Established internationally recognised high standards (‘best practice’) of veterinary clinical care for the individual patient were always followed and/or this work involved the use of cadavers. Ethical approval from a committee was therefore not specifically required for publication in JFMS. Although not required, where ethical approval was still obtained, it is stated in the manuscript.

Informed consent

Informed consent (verbal or written) was obtained from the owner or legal custodian of all animal(s) described in this work (experimental or non-experimental animals, including cadavers) for all procedure(s) undertaken (prospective or retrospective studies). No animals or people are identifiable within this publication, and therefore additional informed consent for publication was not required.

ORCID iD

Kristina A Lederer

Supplementary material

The following files are available online:

Table 1: Clinical pathology results.

Table 2: History and physical examination findings.

References

Hill

Winkle

. Acute necrotizing pancreatitis and acute suppurative pancreatitis in the cat. J Vet Intern Med 1993; 7: 25–33.

De Cock

HEV

Forman

Farver

, et al. Prevalence and histopathologic characteristics of pancreatitis in cats. Vet Pathol 2007; 44: 39–49.

Ferreri

Hardam

Kimmel

, 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.

Steiner

Williams

. Feline exocrine pancreatic disorders. Vet Clin North Am Small Anim Pract 1999; 29: 551–575.

Schermerhorn

Pembleton-Corbett

Kornreich

. Pulmonary thromboembolism in cats. J Vet Intern Med 2004; 18: 533–535.

Estrin

Wehausen

Lessen

, et al. Disseminated intravascular coagulation in cats. J Vet Intern Med 2006; 20: 1334–1339.

Balthazar

Robinson

Megibow

, et al. Acute pancreatitis: value of CT in establishing prognosis. Radiology 1990; 174: 331–336.

French

Twedt

Rao

, et al. Computed tomographic angiography and ultrasonography in the diagnosis and evaluation of acute pancreatitis in dogs. J Vet Intern Med 2018; 15364.

Etue

Penninck

Labato

, et al. Ultrasonography of the normal feline pancreas and associated anatomic landmarks: a prospective study of 20 cats. Vet Radiol Ultrasound 2001; 42: 330–336.

10.

Hecht

Henry

. Sonographic evaluation of the normal and abnormal pancreas. Clin Tech Small Anim Pract 2007; 22: 115–121.

11.

Williams

Panciera

Larson

, et al. Ultrasonographic findings of the pancreas in cats with elevated serum pancreatic lipase immunoreactivity. J Vet Intern Med 2013; 27: 913–918.

12.

Oppliger

Hartnack

Reusch

, et al. Agreement of serum feline pancreas-specific lipase and colorimetric lipase assays with pancreatic ultrasonographic findings in cats with suspicion of pancreatitis: 161 cases (2008–2012). J Am Vet Med Assoc 2014; 244: 1060–1065.

13.

Crain

Sharkey

Cordner

, et al. Safety of ultrasound-guided fine-needle aspiration of the feline pancreas: a case-control study. J Feline Med Surg 2015; 17: 858–863.

14.

Simpson

Shiroma

Biller

, et al. Ante mortem diagnosis of pancreatitis in four cats. J Small Anim Pract 1994; 35: 93–99.

15.

Saunders

. Ultrasonography of the pancreas. Probl Vet Med 1991; 3: 583–603.

16.

Saunders

VanWinkle

Drobatz

, 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.

17.

Weiss

Gagne

Armstrong

. Relationship between inflammatory hepatic disease and inflammatory bowel disease, pancreatitis, and nephritis in cats. J Am Vet Med Assoc 1996; 209: 1114–1116.

18.

Wakeling

Moore

Elliott

, et al. Diagnosis of hyperthyroidism in cats with mild chronic kidney disease. J Small Anim Pract 2008; 49: 287–294.

19.

Schreurs

Vermote

Barberet

, et al. Ultrasonographic anatomy of abdominal lymph nodes in the normal cat: ultrasound of feline abdominal lymph nodes. Vet Radiol Ultrasound 2008; 49: 68–72.

20.

Leveille

Biller

Shiroma

. Sonographic evaluation of the common bile duct in cats. J Vet Intern Med 1996; 10: 296–299.

21.

Hittmair

Vielgrader

Loupal

. Ultrasonographic evaluation of gallbladder wall thickness in cats. Vet Radiol Ultrasound 2001; 42: 149–155.

22.

Zwingenberger

Marks

Baker

, et al. Ultrasonographic evaluation of the muscularis propria in cats with diffuse small intestinal lymphoma or inflammatory bowel disease. J Vet Intern Med 2010; 24: 289–292.

23.

Lund

Armstrong

Kirk

, et al. Health status and population characteristics of dogs and cats examined at private veterinary practices in the United States. J Am Vet Med Assoc 1999; 214: 1336–1341.

24.

Cunningham

Klein

(eds). Cunningham’s textbook of veterinary physiology. 5th ed. St Louis, MO: Elsevier/Saunders, 2013.

25.

Eggleton

Shuster

. Glucose and phosphate excretion in the cat. J Physiol 1954; 124: 613–622.

26.

Cook

. Monitoring methods for dogs and cats with diabetes mellitus. J Diabetes Sci Technol 2012; 6: 491–495.

27.

Crenshaw

Peterson

Heeb

, et al. Serum fructosamine concentration as an index of glycemia in cats with diabetes mellitus and stress hyperglycemia. J Vet Intern Med 1996; 10: 360–364.

28.

Peterson

Melian

Nichols

. Measurement of serum concentrations of free thyroxine, total thyroxine, and total triiodothyronine in cats with hyperthyroidism and cats with nonthyroidal disease. J Am Vet Med Assoc 2001; 218: 529–536.

29.

Akol

Washabau

Saunders

, et al. Acute pancreatitis in cats with hepatic lipidosis. J Vet Intern Med 1993; 7: 205–209.

30.

Penninck

d’Anjou

M-A

(eds). Atlas of small animal ultrasonography. 2nd ed. Ames, IA: John Wiley & Sons, 2015.

31.

Hess

Kass

Shofer

, et al. Evaluation of risk factors for fatal acute pancreatitis in dogs. J Am Vet Med Assoc 1999; 214: 46–51.

32.

Maier

. Echographic patterns of just evolving acute pancreatitis: an experimental study. Eur J Radiol 1990; 11: 145–149.

33.

Simpson

Lamb

. Acute pancreatitis in the dog. In Pract 1995; 17: 328–337.

34.

Lamb

Simpson

. Ultrasonographic findings in cholecystokinin-induced pancreatitis in dogs. Vet Radiol Ultrasound 1995; 36: 139–145.

35.

Sugiyama

Wada

Atomi

, et al. Diagnosis of acute pancreatitis: value of endoscopic sonography. Am J Roentgenol 1995; 165: 867–872.

36.

Arvanitakis

Koustiani

Gantzarou

, et al. Staging of severity and prognosis of acute pancreatitis by computed tomography and magnetic resonance imaging – a comparative study. Dig Liver Dis 2007; 39: 473–482.

37.

Adrian

Twedt

Kraft

, et al. Computed tomographic angiography under sedation in the diagnosis of suspected canine pancreatitis: a pilot study. J Vet Intern Med 2015; 29: 97–103.

38.

Forman

Marks

Cock

HEV

, et al. Evaluation of serum feline pancreatic lipase immunoreactivity and helical computed tomography versus conventional testing for the diagnosis of feline pancreatitis. J Vet Intern Med 2004; 18: 807–815.

39.

Gerhardt

Steiner

Williams

, et al. Comparison of the sensitivity of different diagnostic tests for pancreatitis in cats. J Vet Intern Med 2001; 15: 329–333.

40.

Marolf

Kraft

Dunphy

, et al. Magnetic resonance (MR) imaging and MR cholangiopancreatography findings in cats with cholangitis and pancreatitis. J Feline Med Surg 2013; 15: 285–294.

41.

Rademacher

Ohlerth

Scharf

, et al. Contrast-enhanced power and color Doppler ultrasonography of the pancreas in healthy and diseased cats. J Vet Intern Med 2008; 22: 1310–1316.

42.

Golea

Badea

Socaciu

, et al. Quantitative analysis of tissue perfusion using contrast-enhanced transabdominal ultrasound (CEUS) in the evaluation of the severity of acute pancreatitis. Med Ultrason 2010; 12: 198–204.

43.

Lim

Nakamura

Morishita

, et al. Quantitative contrast-enhanced ultrasonographic assessment of naturally occurring pancreatitis in dogs. J Vet Intern Med 2015; 29: 71–78.

44.

Rademacher

Schur

Gaschen

, et al. Contrast-enhanced ultrasonography of the pancreas in healthy dogs and in dogs with acute pancreatitis: contrast-enhanced ultrasound in canine pancreatitis. Vet Radiol Ultrasound 2016; 57: 58–64.

45.

Worthen

Beabeau

. Normal pancreatic echogenicity: relation to age and body fat. Am J Roentgenol 1982; 139: 1095–1098.

46.

Glaser

Stienecker

. Pancreas and aging: a study using ultrasonography. Gerontology 2000; 46: 93–96.

47.

Choi

. Associated factors for a hyperechogenic pancreas on endoscopic ultrasound. World J Gastroenterol 2010; 16: 4329–4334.

48.

Lee

Kim

Jun

, et al. Clinical implications of fatty pancreas: correlations between fatty pancreas and metabolic syndrome. World J Gastroenterol 2009; 15: 1869–1875.

49.

Naranje

Manchanda

. ‘The dark pancreas’: classic CT appearance of total pancreatic lipomatosis. BMJ Case Rep 2017: bcr-2017-219796. DOI: 10.1136/bcr-2017-219796.

50.

Muresan

Beteg

Lelescu

, et al. Extensive fatty replacement of the pancreas (pancreatic lipomatosis) in a dog. J Comp Pathol 2019; 173: 19–23.

51.

Granger

Hilferty

Francis

, et al. Variability in the ultrasonographic appearance of the pancreas in healthy dogs compared to dogs with hyperadrenocorticism: pancreatic variability on ultrasound in dogs. Vet Radiol Ultrasound 2015; 56: 540–548.

52.

Larson

Panciera

Ward

, et al. Age-related changes in the ultrasound appearance of the normal feline pancreas. Vet Radiol Ultrasound 2005; 46: 238–242.

53.

Stockhaus

Teske

Schellenberger

, et al. Serial serum feline pancreatic lipase immunoreactivity concentrations and prognostic variables in 33 cats with pancreatitis. J Am Vet Med Assoc 2013; 243: 1713–1718.

54.

Marolf

Leach

Gibbons

, et al. Ultrasonographic findings of feline cholangitis. J Am Anim Hosp Assoc 2012; 48: 36–42.

55.

Hellyer

Rodan

Brunt

, et al. AAHA/AAFP pain management guidelines for dogs and cats. J Feline Med Surg 2007; 9: 466–480.

56.

Kwon

Banks

. How should acute pancreatitis be diagnosed in clinical practice? In: Domnguez-Muoz

Malfertheiner

(eds). Clinical pancreatology. Oxford: Blackwell Publishing, 2004, pp 34–39.

57.

Bradley

. Pancreatic duct pressure in chronic pancreatitis. Am J Surg 1982; 144: 313–316.

58.

Karanjia

Singh

Widdison

, et al. Pancreatic ductal and interstitial pressures in cats with chronic pancreatitis. Dig Dis Sci 1992; 37: 268–273.

59.

Karanjia

Widdison

Leung

, et al. Compartment syndrome in experimental chronic obstructive pancreatitis: effect of decompressing the main pancreatic duct. Br J Surg 1994; 81: 259–264.

60.

di Mola

Friess

Martignoni

, et al. Connective tissue growth factor is a regulator for fibrosis in human chronic pancreatitis. Ann Surg 1999; 230: 63–71.

61.

Di Sebastiano

Fink

Weihe

, et al. Immune cell infiltration and growth-associated protein 43 expression correlate with pain in chronic pancreatitis. Gastroenterology 1997; 112: 1648–1655.

62.

Armstrong

Williams

. Pancreatitis in cats. Top Companion Anim Med 2012; 27: 140–147.

63.

Xenoulis

Steiner

. Canine and feline pancreatic lipase immunoreactivity. Vet Clin Pathol 2012; 41: 312–324.

64.

Bazelle

Watson

. Pancreatitis in cats: is it acute, is it chronic, is it significant? J Feline Med Surg 2014; 16: 395–406.

Supplementary Material

Please find the following supplemental material available below.

For Open Access articles published under a Creative Commons License, all supplemental material carries the same license as the article it is associated with.

For non-Open Access articles published, all supplemental material carries a non-exclusive license, and permission requests for re-use of supplemental material or any part of supplemental material shall be sent directly to the copyright owner as specified in the copyright notice associated with the article.

0.00 MB

0.03 MB

0.01 MB