Recurrent pancreatic abscesses coexisting with a suspected adenocarcinoma in a cat

Abstract

Case summary

A 13-year-old neutered female domestic shorthair cat was referred for weight loss, polyphagia, polyuria, polydipsia and intermittent vomiting. Blood work demonstrated diabetes mellitus; abdominal ultrasonography revealed a hypoechoic, thickened pancreas with two large fluid-filled cavities within the body and right limb. Cytology of the aspirated fluid indicated suppurative inflammation with bacterial infection, which cultured Pasteurella multocida. Medical management for diabetes mellitus and pancreatic abscessation was initiated. After approximately 4 months of antimicrobial therapy and five percutaneous drainages, clinical signs improved; nevertheless, serial abdominal ultrasonography demonstrated persistent pancreatic abscessation, while repeated cultures and antibiograms documented progressively resistant bacterial infections. The condition culminated in abscess rupture and septic peritonitis, prompting surgical drainage and omentalisation. Histopathological examination of the pancreatic parenchyma revealed severe lymphoplasmacytic pancreatitis with glandular atrophy, while evaluation of the pancreatic tissue associated with the abscess demonstrated a suspected pancreatic exocrine neoplasm, most compatible with a well-differentiated adenocarcinoma.

Relevance and novel information

This case highlights the need for earlier consideration of surgical intervention in cases of recurrent pancreatic abscessation and underscores the importance of including concurrent pancreatic neoplasia as a differential diagnosis in chronic, non-resolving presentations.

Case description

A 13-year-old, neutered female domestic shorthair cat was referred for a 2-month history of progressive weight loss, polyuria, polydipsia and polyphagia (PU/PD/PP), intermittent vomiting and diarrhoea. On presentation, the cat had a World Small Animal Veterinary Association body condition score (BCS) of 2/9 with marked muscle wasting. Physical examination identified a firm cranial abdominal midline mass eliciting mild discomfort on palpation; rectal temperature and vital parameters were within normal limits.

Initial laboratory evaluation for PU/PD/PP included serum biochemistry and urinalysis, demonstrating fasting hyperglycaemia and marked glycosuria (4+) without appreciable ketonuria (Table 1). Given the poor BCS, despite polyphagia, serum cobalamin concentration was measured in-house, revealing hypocobalaminaemia (Table 1), while fructosamine, feline trypsin-like immunoreactivity and total thyroxine were submitted to a reference laboratory.

Table 1.

Biochemical results at the first visit

Parameter	Values	RI
Urea (mmol/l)	8.8	5.7–12.9
Creatinine (µmol/l)	83	71–212
Blood urea nitrogen:creatinine ratio	26	–
Phosphate (mmol/l)	1.7	1.0–2.4
Calcium (mmol/l)	2.4	2–2.8
Total bilirubin (µmol/l)	5	0–15
Alanine aminotransferase (IU/l)	89	12–130
Alkaline phosphatase (IU/l)	67	14–111
Gamma-glutamyl transferase (IU/l)	2	0–4
Glucose (mmol/l)	14.9	4.0–8.8
Total cholesterol (mmol/l)	5.1	1.7–5.8
DGGR lipase (IU/l)	637	100–1400
Total protein (g/l)	79	57–89
Albumin (g/l)	27	23–39
Globulin (g/l)	53	28–51
Albumin:globulin ratio	0.5	–
Cobalamin (vitamin B12) (ng/l)	<75	290–1500

Values in bold are outside the reference interval (RI)

Abdominal ultrasonography (US), performed under sedation with methadone (0.2 mg/kg IV, Comfortan; Dechra), identified two large cavitary lesions within the right limb and body of the pancreas (3.2 cm × 3 cm and 3.4 cm × 3.3 cm), with thickened hyperechoic walls containing hypoechoic fluid and echogenic debris (Figure 1a,b). The pancreas was diffusely enlarged (≈2 cm) and hypoechoic, with hyperechoic peripancreatic fat and a mild anechoic peritoneal effusion. Concurrent findings included a hyperechoic liver, gallbladder wall thickening, diffuse intestinal muscularis thickening with hyperechoic striations and mild generalised abdominal lymphadenopathy.

Figure 1.

Abdominal ultrasound findings. Two large, rounded cavitary lesions, characterised by irregular, thickened and hyperechoic walls and filled with echogenic particulate fluid, are identified in the right limb and body of the pancreas. The lesions measure approximately (a) 3.2 cm × 3 cm and (b) 3.4 cm × 3.3 cm, and significantly distort the organ’s contour

US-guided fine-needle aspiration (FNA) yielded 22 ml of purulent fluid from the two pancreatic lesions. Despite the immediate post-drainage collapse of the cavities, rapid re-accumulation occurred within minutes. Cytology demonstrated degenerated neutrophils with bacterial rods, and culture yielded profuse growth of Pasteurella multocida. Pancreatic body cytology revealed marked neutrophilic inflammation, while the abdominal fluid was classified as a high-protein transudate. Findings were consistent with pancreatitis and pancreatic abscesses (PAs). Concurrent abnormalities raised suspicion for triaditis or hepatobiliary disease, as well as primary intestinal disease (eg, chronic inflammatory enteropathy or small-cell lymphoma), with associated lymphadenopathy.

Given the cat’s poor BCS and suspected diabetes mellitus (DM), conservative management of the PAs was initiated with antimicrobials and percutaneous drainage. The cat was discharged with amoxicillin-clavulanate (12.5 mg/kg PO q12h, Clavaseptin; Vetoquinol), a hydrolysed protein diet (Purina Pro Plan Veterinary Diets HA Hypoallergenic; Nestlé Purina PetCare), cobalamin supplementation (cyanocobalamin and folic acid 250 µg/cat PO q24h, Cobalaplex; Protexin Veterinary) and buprenorphine (0.02 mg/kg transmucosally q8h, Buprecare; Animalcare) to be administered on an as-needed basis for signs of pain. Anti-hyperglycaemic therapy was withheld pending reference results.

At the 2-week re-evaluation, PU/PD and vomiting persisted. Reference laboratory results confirmed DM and excluded hyperthyroidism and exocrine pancreatic insufficiency (Table 2). Repeated abdominal US, performed under the same sedation protocol, demonstrated persistent PAs without appreciable size reduction and otherwise unchanged findings. Drainage cytology and culture identified neutrophilic inflammation with bacterial rods and cocci, and moderate growth of P multocida, susceptible to all tested antimicrobials. Marbofloxacin (2 mg/kg PO q24h, Marbocyl P; Vetoquinol) was added to the antimicrobial regimen owing to its favourable tissue distribution. ¹ Recombinant human protamine zinc insulin (0.25 IU/kg SC q12h, ProZinc; Boehringer Ingelheim) was started at home but discontinued after 9 days owing to poor patient tolerance for injections; therapy transitioned to velagliflozin (1 mg/kg PO q24h, Senvelgo; Boehringer Ingelheim), with glycaemic monitoring via in-clinic blood glucose curves.

Table 2.

Feline trypsin-like immunoreactivity, total thyroxine and fructosamine results

Parameter	Values	RI
Feline trypsin-like immunoreactivity (µg/l)	34.7	12–82
Total thyroxine (nmol/l)	21	15–50
Fructosamine (nmol/l)	508	190–350

Values in bold are outside the reference interval (RI)

Over the following 2 months, the cat gained 18% in body weight, with resolution of PU/PD/PP, and effective glycaemic control. Despite clinical improvement, serial abdominal US showed persistent PAs, with ongoing neutrophilic inflammation on repeated cytology; however, no bacteria were identified and cultures were not performed.

On day 70, culture of the PAs yielded profuse growth of multidrug-resistant Enterococcus faecium. Surgical intervention was recommended but deferred owing to financial constraints, with the intention to pursue it once feasible. Meanwhile, medical management was maintained unchanged until completion of the antimicrobial course; antimicrobial therapy was then discontinued to minimise further antimicrobial resistance before surgery.

On day 112, the cat presented with lethargy, pyrexia (39.5°C), hypotension (90/60 mmHg; mean arterial pressure 66 mmHg) and relative bradycardia (140–160 bpm). Cardiac auscultation revealed a grade II/VI systolic murmur with a gallop rhythm. Biochemistry and haematology results are summarised in Table 3. Abdominal US confirmed persistent abscessation of the right pancreatic limb and an irregular discontinuity of the pancreatic body, suggestive of abscess rupture, with a small volume of echogenic peritoneal fluid. Effusion cytology demonstrated mixed neutrophilic-macrophagic inflammation, raising concern for septic peritonitis; culture of the PAs yielded alpha-haemolytic Streptococcus species, sensitive only to clindamycin and potentiated sulphonamides.

Table 3.

Haematology and biochemistry results after the development of septic peritonitis

Parameter	Values	RI
Red blood cells (t/l)	6.9	6.5–12.2
Haematocrit (l/l)	35.6	30.3–52.3
Haemoglobin (mmol/l)	11.3	9.8–16.2
Reticulocytes (%)	0.9	–
Reticulocytes (absolute) (g/l)	64.5	3–50
Total white blood cells (g/l)	20.7	2.9–17.0
Neutrophils (%)	79.3	–
Lymphocytes (%)	9.8	–
Monocytes (%)	6.8	–
Eosinophils (%)	3.7	–
Basophils (%)	0.4	–
Neutrophils (absolute) (m/l)	16.4	2.3–10.3
Lymphocytes (absolute) (m/l)	2.0	0.9–6.9
Monocytes (absolute) (m/l)	1.4	0.1–0.7
Eosinophils (absolute) (m/l)	0.8	0.2–1.6
Basophils (absolute) (m/l)	0.1	0.1–0.3
Platelets (g/l)	326	151–600
Urea (mmol/l)	14.1	5.7–12.9
Creatinine (µmol/l)	111	71–212
Blood urea nitrogen:creatinine ratio	31	–
Phosphate (mmol/l)	1.9	1.0–2.4
Sodium (mmol/l)	159	150–165
Potassium (mmol/l)	3.0	3.5–5.8
Sodium:potassium ratio	53	–
Chloride (mmol/l)	112	112–129
Calcium (mmol/l)	2.5	2.0–2.8
Total bilirubin (µmol/l)	3	0–15
Alanine aminotransferase (IU/l)	88	12–130
Alkaline phosphatase (IU/l)	41	14–111
Gamma-glutamyl transferase (IU/l)	0	0–4
Glucose (mmol/l)	8.2	4.0–8.8
Total cholesterol (mmol/l)	4.2	1.7–5.8
DGGR lipase (IU/l)	905	100–1400
Total protein (g/l)	81	57–89
Albumin (g/l)	29	23–39
Globulin (g/l)	52	28–51
Albumin:globulin ratio	0.6	–

Values in bold are outside the reference interval (RI)

Immediate surgical exploration and abdominal lavage, although considered optimal management, were deemed high risk owing to cardiovascular instability; therefore, initial medical stabilisation was undertaken, with surgery planned once stabilisation was achieved. Hypotension responded promptly to intravenous crystalloid boluses, followed by a continuous Hartmann’s solution supplemented with potassium chloride; vasopressor support was not required. Heart rate was closely monitored, with glycopyrrolate available but not administered. Concurrent therapy is summarised in Table 4.

Table 4.

Concurrent medical therapy during stabilisation

Drug	Dose	Route	Administration frequency
Clindamycin	12.5 mg/kg	IV	q12h
Methadone	0.2 mg/kg	IV	q4h
Ketamine*	5 µg/kg/min	IV CRI	Overnight
Velagliflozin	1 mg/kg	PO	q24h
Maropitant	1 mg/kg	IV	q24h
Purina hydrolysed diet	25–50% of RER	PO	q4h assisted feeding

^*Ketavet; MSD Animal Health

CRI = constant rate infusion; IV = intravenous; PO = per os; RER = resting energy requirement

After 5 days of hospitalisation, the cat became cardiovascularly stable and normokalaemic (4.1 mmol/l, reference interval 3.5–5.8), and exploratory laparotomy was performed. Intraoperatively, the pancreas appeared diffusely abnormal with multifocal millimetric white nodules and a large, thick-walled, fluid-filled lesion in the right pancreatic limb. Histopathology of the left limb demonstrated severe chronic interstitial and periductal lymphoplasmacytic and neutrophilic pancreatitis with marked fibrosis and glandular atrophy (Figure 2a,b). A 10 mm biopsy adjacent to the abscess cavity revealed atypical epithelial cells of exocrine pancreatic origin, most compatible with a well-differentiated acinar-type adenocarcinoma ² (Figure 3a,b). Although adenoma or marked hyperplasia were considered differential diagnoses, the presence of architectural irregularity, mitotic activity and peripheral infiltrative growth within reactive fibrous stroma supported a neoplastic process. Immunohistochemistry was not performed, as it was unlikely to add diagnostic value for an exocrine pancreatic lesion; this is acknowledged as a limitation of this report.

Figure 2.

Representative histological sections of the left pancreatic limb at low (scale bar 1 mm) and medium (scale bar 100 µm) magnification, stained with haematoxylin and eosin. (a) The periductal and interstitial stroma is markedly expanded by fibrosis, creating a micronodular appearance at subgross examination. Entrapped lobules of exocrine pancreas are inflamed and multifocally isolated and atrophied. These features are consistent with chronic periductal and interstitial pancreatitis with marked fibrosis. Numerous residual areas of exocrine pancreas, including acinar cells, are present alongside dilated, inflamed and likely proliferative ducts. (b) Cords of epithelial cells are embedded in fibrotic and inflamed stroma

Figure 3.

Representative histological sections of the pancreatic parenchyma and pancreatic tissue adjacent to the abscess cavity at medium (scale bar 100 µm) and high (scale bar 50 µm) magnification, stained with haematoxylin and eosin. (a) The pancreatic parenchyma is replaced by an atypical proliferation of exocrine pancreatic epithelial cells forming variably distinct tubular and acinar structures, multifocally associated with small accumulations of eosinophilic material. This proliferation is supported by a fine fibrous stroma, which is moderately inflamed and contains neutrophils, lymphocytes and plasma cells. (b) The atypical epithelial cells are consistent with exocrine pancreatic origin and are cuboidal to columnar with indistinct cell borders. They contain a moderate amount of eosinophilic cytoplasm, often with distinct, brightly eosinophilic granules, and exhibit mild to moderate anisocytosis and anisokaryosis. Occasional mitotic figures are also observed

Postoperative management mirrored the preoperative medical regimen (Table 4), with the addition of gabapentin (10 mg/kg PO q12h, Neurontin; Pfizer). Despite initial improvement, the cat deteriorated 4 days later, developing pyrexia and abdominal effusion, and was humanely euthanased at the owners’ request. Post-mortem examination was declined.

Discussion

Pancreatic abscesses are rare findings in veterinary medicine, particularly in cats,^3,4 and are defined as circumscribed purulent collections within the pancreatic parenchyma, typically arising as a sequela of severe necrotising or chronic-active pancreatitis.^3–6 They may be either sterile or infected. ⁷ In the present case, serial cultures yielded P multocida, E faecium and alpha-haemolytic Streptococcus, findings that contrast with the canine literature ⁷ but align with feline and human reports, where microbial agents are commonly detected.^3,4,8 This discrepancy may reflect anatomical similarities between feline and human gastrointestinal (GI) systems, in which the bile and pancreatic ducts converge at a common duodenal papilla, predisposing to translocation of intestinal bacteria and pancreatic inflammation. ⁹ Pancreatitis in cats has also been reported to occur secondary to systemic bacteraemia or portal venous spread. ⁹

The infection’s aetiology remains uncertain. P multocida, a commensal of the feline respiratory tract, ¹⁰ may have reached the pancreas via haematogenous spread or, less likely, after an abdominal bite wound. Enterococcus and Streptococcus species, commensals of the GI tract,^11–15 may instead have translocated through the shared bile and pancreatic ducts, as supported by experimental models demonstrating Escherichia coli migration from the intestine into inflamed pancreatic tissue. ¹⁶ Notably, progressive colonisation by increasingly resistant bacterial strains on serial culture reflects an evolutionary pattern often observed in nosocomial infections. ¹⁷

Additional comorbidities included DM, a condition reported only once in association with PAs in cats. ³

At the first referral visit, anti-hyperglycaemic therapy was deferred pending fructosamine results, despite findings already strongly suggestive of DM, as concurrent exocrine pancreatic disease remained a plausible alternative explanation for weight loss, polyphagia and gastrointestinal signs, and the patient showed no ketonuria or other evidence of metabolic decompensation. Although this approach was considered clinically justifiable at the time, recently published iCatCare consensus guidelines ¹⁸ suggest that earlier initiation of anti-hyperglycaemic therapy may also have been warranted.

In the present case, DM was likely multifactorial. Histopathology demonstrated severe interstitial pancreatic fibrosis, supporting potential pancreatic endocrine injury, whereas systemic inflammation may have contributed via cytokine-mediated peripheral insulin resistance.^19,20 Favourable glycaemic response to velagliflozin further suggests the presence of residual endogenous insulin secretion. Although current guidelines favour home-based monitoring, including continuous interstitial glucose measurement, ²¹ glycaemic status during initial stabilisation was assessed using serial in-clinic blood glucose curves, which may be affected by stress-induced hyperglycaemia. In addition, ketone monitoring, recommended during sodium-glucose cotransporter-2 inhibitor therapy, was not performed serially and is acknowledged as a limitation of the case.

Management of PAs in cats is poorly documented.^3,4,6 US-guided percutaneous drainage combined with antimicrobial therapy is a first-line treatment in human medicine for high-risk surgical patients, delaying or obviating surgery in over 90% of cases with low complication rates.^22,23 This approach has also been reported to be safe in cats, supporting the feasibility of repeated minimally invasive pancreatic drainage. ²⁴ In the present case, conservative management was pursued owing to poor BCS and comorbidities; surgical intervention was recommended after failure of medical management and the emergence of multidrug-resistant bacteria, but declined because of owner-related constraints. Subsequent deterioration with septic peritonitis necessitated surgical exploration, which revealed a suspected pancreatic adenocarcinoma coexisting with the residual abscess.

Exocrine pancreatic neoplasms are rare in companion animals (<0.5% of all cancers).^25–27 Adenocarcinomas represent the most reported malignant subtype in cats, and typically arise from ductal epithelium, although acinar origin has also been described.^28,29

Predisposing factors for pancreatic cancer, as outlined in both the human and veterinary literature, include chronic pancreatitis, pancreatic inflammation and DM, with the latter increasing predisposition by up to 50% in humans. ³⁰ Conversely, pancreatic neoplasia is an extremely rare cause of acute pancreatitis and pancreatic cystic formation, with only one case report documenting an adenocarcinoma as the underlying cause of a pancreatic pseudocyst in a cat. ³¹ In this case, the absence of metastatic disease on serial imaging during the 4-month interval between PA identification and surgery, despite reported metastatic rates of up to 80% at adenocarcinoma diagnosis,^26,27 raises the possibility of secondary neoplastic development in the context of chronic pancreatic inflammation and DM.

Ultrasonographic features of pancreatic adenocarcinoma typically include well-defined, cavitary or heterogeneous masses. ³² However, in histologically diffuse forms, the pancreas may appear uniformly enlarged and hypoechoic, mimicking inflammatory disease. ³² Comparable diagnostic challenges have been reported in human medicine, where adenocarcinoma, coexisting with an abscess, remained undetected despite advanced imaging, including CT.^33,34

Diagnosis typically relies on US-guided FNA or biopsy. ³⁵ However, the limited cellular exfoliation of adenocarcinoma reduces sensitivity, and definitive diagnosis is often only achieved through surgical biopsy or post-mortem histopathology. ³⁵

Treatment of pancreatic adenocarcinoma in cats is limited because of the rapid progression of the disease. ³⁶ Nevertheless, when detected at an early and localised stage, surgical resection with or without adjuvant therapy has been reported to extend median survival to 316.5 days (range 25–964). ³⁷

Needle tract seeding (NTS) after FNA of pancreatic neoplastic lesions has rarely been reported in cats with adenocarcinoma ³⁸ and is considered a rare complication in both veterinary and human medicine.^39,40 In the present case, the timing of adenocarcinoma development is unknown; therefore, it cannot be determined whether the absence of NTS reflects late tumour onset or the overall rarity of this complication.

Concurrent ultrasonographic findings were suggestive of triaditis or hepatobiliary disease, primary intestinal disorders and multifocal lymphadenopathy. However, the absence of histopathological confirmation limited the ability to definitively confirm associated conditions or the presence of any metastatic spread.

Conclusions

This report describes an unusual presentation of chronic suppurative pancreatitis with PAs in a diabetic cat, ultimately associated with the development of a suspected pancreatic adenocarcinoma.

Management of pancreatic abscessation in cats remains controversial. Prolonged conservative therapy in this instance provided only symptomatic relief, failed to achieve resolution and contributed to the emergence of multidrug-resistant bacterial infections. This approach likely prolonged the disease course and delayed surgical intervention, potentially allowing secondary neoplastic transformation to occur in the context of persistent pancreatic inflammation and DM, both recognised predisposing factors.

This case highlights the limitations of prolonged medical management and the importance of considering concurrent pancreatic pathology in cases of chronic, non-resolving abscessation, even in the absence of supportive ultrasonographic or cytological evidence. Recognition of this rare but life-threatening association may facilitate earlier diagnosis, timely intervention and appropriate treatment.