Pancreatitis in Dogs

What is pancreatitis in dogs?

Inflammatory disorder of the exocrine pancreas (acute or chronic); most common exocrine pancreatic disease in dogs. Pathology may be focal or diffuse; clinical severity ranges from subclinical to life‑threatening.

Name key precipitating factors and the workup implication.

Underlying causes include hypertriglyceridemia, endocrinopathies (hyperadrenocorticism, hypothyroidism, ± diabetes), drugs/toxins, high‑fat diets, trauma, infectious and immune‑mediated syndromes. Most are cryptogenic, but evaluate especially in recurrent cases (e.g., fasted triglycerides, endocrine testing, drug review).

Typical clinical signs of canine pancreatitis.

Cranial abdominal pain, vomiting, inappetence, lethargy; diarrhea and nausea are common. Chronic disease may present as low‑grade, intermittent GI signs with waxing/waning course.

Core treatment pillars for pancreatitis.

Supportive care: fluids, early nutrition, opioid analgesia, antiemetics. Consider fuzapladib sodium IV for acute onset cases (LFA‑1 inhibitor, 0.4 mg/kg IV q24h × 3 doses, dogs ≥6 months).

What is the overall prognosis for dogs with pancreatitis?

Highly variable; most survive acute and chronic episodes. Recurrences are reported; chronic disease can lead to EPI and/or diabetes mellitus due to parenchymal loss.

Where is the canine pancreas and what are its functions?

Cranial abdomen between transverse colon and greater curvature of stomach. ~90% exocrine acini (digestive enzymes, bicarbonate, intrinsic factor); ~10% endocrine islets (insulin/glucagon etc.). Close anatomic/functional ties mean exocrine and endocrine diseases can co‑occur.

How is pancreatic secretion triggered?

Food presence, gastric distension, and fat/protein in small intestine via hormones (CCK, secretin), enteric nervous system, and vagus. Failure → maldigestion and malabsorption.

Summarize the pathophysiology of pancreatitis.

Premature intra‑acinar activation of zymogens (trypsinogen→trypsin) overwhelms protective mechanisms (PSTI/SPINK1; trypsin autolysis), leading to autodigestion, fat necrosis, local/systemic inflammation, and possibly SIRS/MODS.

What is the 'critical threshold' theory in pancreatitis?

Disease emerges when cumulative stressors exceed protective mechanisms; explains why some dogs remain subclinical while others develop severe disease.

Which organ systems can be affected in pancreatitis?

Mild acute: primarily exocrine pancreas. Severe acute: multiorgan dysfunction (hepatobiliary, kidneys, lungs, heart) and DIC. Chronic: exocrine and endocrine loss → EPI and/or diabetes mellitus when ~80–90% of pancreatic mass lost.

How are diabetes mellitus and pancreatitis related?

Bidirectional: end‑stage chronic pancreatitis may underlie ~30% of canine DM; pre‑existing DM may predispose to acute pancreatitis. Course varies; exocrine and endocrine decline often parallel.

How common is chronic pancreatitis on necropsy? Clinical caveat?

~1/3 of dogs may show histologic chronic pancreatitis at necropsy, but many lack clinical signs; clinical significance can be uncertain.

Breeds with reported associations.

Acute: Miniature Schnauzer, Poodle, Yorkshire Terrier, terriers, Alaskan Malamute (single survey).

Chronic: Cavalier King Charles Spaniel, Collie, Boxer. IgG4‑related syndrome: English Cocker Spaniel (blue roan predisposition noted). Comorbidities often present in data.

List key risk factors to screen in suspected/recurrent cases.

Breed predisposition; high‑fat diet/indiscretion; drugs/toxins (e.g., azathioprine, KBr, organophosphates, ± phenobarbital, cholinesterase inhibitors, cholinergic agonists, zinc); endocrinopathies (hypothyroid, hyperadrenocorticism, ± DM); hypertriglyceridemia/cholesterolemia; trauma; obesity; infections (Babesia, Heterobilharzia, Ehrlichia, CPV, leishmaniosis); envenomation; hypercalcemia; ischemia; duct obstruction; surgical manipulation; reflux.

Are corticosteroids a risk factor?

Historical concern, but routine corticosteroid use is no longer considered a definitive risk factor for initiating pancreatitis; interpretation must be contextual.

Common comorbid conditions with pancreatitis.

Endocrinopathies (HAC, hypothyroidism, DM), chronic inflammatory enteropathies, biliary tract disease, reactive hepatopathy, systemic immune‑mediated syndromes (English Cocker), hypertriglyceridemia.

How do acute and chronic pancreatitis relate?

They exist on a continuum. Recurrent acute episodes may progress to chronic disease; many chronic cases are underdiagnosed and may be subclinical until EPI/DM emerges.

CBC patterns in pancreatitis.

Nonspecific: neutrophilia ± left shift; possible thrombocytosis/thrombocytopenia, anemia, hemoconcentration. Always review smear; use to screen for differentials/systemic complications.

Chemistry changes that support/complicate pancreatitis.

↑ALP>ALT (reactive hepatopathy or posthepatic cholestasis from pancreatic compression), hyperbilirubinemia (raises EHBDO concern), ± hypocalcemia, mild hypoalbuminemia, hypercholesterolemia, dysglycemia; azotemia may reflect prerenal or AKI. SDMA may be more sensitive than creatinine for AKI.

When to check triglycerides and CRP.

Fasted triglycerides (12 h) in all pancreatitis cases; moderate/marked hypertriglyceridemia suggests risk and guides diet/pharmacotherapy. CRP often ↑ in acute disease; serial CRP may reflect response but is not routinely used.

Urinalysis and endocrine testing pearls.

UA: AKI patterns, bilirubinuria (EHBDO), proteinuria. Cortisol/ACTH stim to rule out hypo‑A in chronic/recurrent GI signs (prevalence low). Avoid HAC testing during acute illness.

Principles of pancreatic lipase testing.

Elevated pancreatic lipase (concentration or activity) supports pancreatitis but is not definitive; can be elevated in non‑pancreatic disease (secondary pancreatic inflammation). Interpret with imaging and clinical context.

Recognize false positives/negatives with lipase tests.

False positives: portal hypertension, CHF (hepatic congestion), steroid therapy, acute abdomen without pancreatitis.

False negatives: chronic pancreatitis (fibrosis/atrophy), mild acute disease, delayed sampling (short half‑life ~48 h).

When is serial cPLI useful?

In recurrent suspected pancreatitis to support diagnosis, trend severity, and assess response to therapy; also useful when repeat imaging is impractical. Do not substitute for clinical improvement.

When to repeat imaging.

If clinically improving, repeat US in ~4 weeks. If worsening/not responding, repeat sooner to assess for abscess, effusion, or alternate pathology. Persistent or mass‑like changes → consider cytology/histopath.

What is EHBDO and how is it seen?

Extrahepatic bile duct obstruction secondary to pancreatitis; suggested by hyperbilirubinemia and duct dilation on US. Requires close monitoring and sometimes intervention.

CT/CTA in pancreatitis—why and when?

Contrast CT (especially angiography) can better identify severe disease patterns and portal vein thrombosis than US, potentially altering therapy/prognosis. Consider in severe cases or when thrombi suspected.

When to sample the pancreas? Risks?

US‑guided FNA/biopsy considered for mass effect, suspected abscess/pseudocyst, or to exclude neoplasia; complication rate reported low (~6%). Sampling does not meaningfully raise cPLI. Histopath confirms acute vs chronic but may not correlate with severity and is rarely required.

Corticosteroids: when to consider and when to avoid.

Low‑dose anti‑inflammatory pred/prednisolone (0.5–1 mg/kg PO q24h) may be considered in refractory severe disease (e.g., persistent hypotension) or EHBDO when surgery contraindicated. Avoid with active GI bleeding or documented sepsis.

Antithrombotic/anticoagulants.

Use if thrombi (e.g., portal vein) are documented by imaging. CTA detects thrombi better than US. No specific pancreatitis‑only risk classification in consensus guidelines; individualize.

How to manage chronic pancreatitis.

Address comorbidities; use low‑fat diet, analgesia, anti‑nausea meds, ± antioxidants (e.g., vitamin E). Immunosuppressants (e.g., prednisone; cyclosporine) only after ruling out infections/comorbidities and ideally with histologic confirmation of lymphocytic inflammation. Taper to lowest effective dose; monitor for insulin resistance.

Management of pseudocysts/abscesses/necrotic regions.

Some resolve with medical therapy; others require drainage or surgery (especially ruptured/infected). No strict criteria distinguish medical vs surgical—use clinical context, imaging, and cytology/culture. Consider referral.

Hypertriglyceridemia management and targets.

Dietary fat restriction (<2 g fat/100 kcal). If inadequate: Fenofibrate 6.5–10 mg/kg PO q12h; Gemfibrozil 10 mg/kg PO q12h; Bezafibrate 4–10 mg/kg PO q24h; add omega‑3s 200–300 mg/kg PO q24h. Aim fasted triglycerides <500 mg/dL (anecdotal).

Managing endocrinopathies and drug‑associated disease.

HAC: trilostane/mitotane; DM: insulin ± diet; hypothyroidism: levothyroxine. For suspect drug‑induced cases, stop unnecessary meds or switch alternatives; document cPLI before/after withdrawal when feasible.

How long should a low‑fat diet be used after an acute episode?

2–4 weeks post‑hospitalization if possible (monitor weight). Long‑term strict fat restriction for dogs with hypertriglyceridemia or recurrent idiopathic disease; otherwise, transition to adult maintenance diet after recovery.

Negative prognostic indicators and complications to monitor.

Worse outcomes associated with SIRS, coagulopathy, ↑creatinine, ionized hypocalcemia, azotemia, local effusions, AKI, ARDS, thromboemboli, myocardial injury, and multiorgan dysfunction.

Outpatient follow‑up cadence.

Recheck/phone at 2–3 days for hydration/apparent appetite/pain; repeat chemistry if significant abnormalities/EHBDO/AKI concerns. At 1–2 weeks: CBC/chemistry and fasted triglycerides; adjust meds. Consider pancreatic lipase monitoring; keep feeding tubes until sustained appetite meets RER.

Which chronic drugs should be paused during active pancreatitis?

Trilostane/mitotane and ACE inhibitors/ARBs during dehydration/hypovolemia or marked anorexia to avoid worsening GI signs and renal perfusion. Restart after recovery.