Acute pancreatitis in two five-day-old Appaloosa foals



Severe acute pancreatitis (SAP) in foals is rare and treatment has not been documented. This paper describes the clinical, haematological and ultrasonographic findings as well as attempted treatment of SAP in two 5-day-old Appaloosa fillies. Clinical signs, including colic, diarrhoea and coma, may be mistaken for sepsis or neonatal encephalopathy. Hyperlipaemic serum and peritoneal fluid, and elevated serum and peritoneal fluid amylase and lipase activities aided the diagnosis. Severe acute pancreatitis should be included as a differential in an acutely ill foal with diarrhoea, colic, cerebral cortical dysfunction and hyperlipaemia.


Severe acute pancreatitis (SAP) has rarely been documented in equids (Baker 1978; Lilley and Beeman 1983; Del Piero et al. 1996; Dacre et al. 2003; Kawaguchi et al. 2004; Bakos et al. 2008; Johnson et al. 2009). There is only one report of this condition in a foal (Taintor et al. 2006), a 3-day-old Quarter Horse filly that became acutely ill and presented for shock and nonresponsive coma and was diagnosed with acute pancreatitis at post mortem examination. A serum sample evaluated later had increased lipase activity.

There is one report of successful treatment of acute pancreatitis in the mature horse (Bakos et al. 2008). Treatment should address the hypovolaemic shock and any predisposing conditions (Andris 2010). The following report describes the clinical, haematological and ultrasonographic findings and treatment of severe acute pancreatitis in two 5-day-old Appaloosa fillies.

Case 1

Case history, clinical and laboratory findings

A 5-day-old Appaloosa filly, healthy for the first 4 days of life with serum immunoglobulin G concentration (IgG) >8.0 g/l as measured by the referring veterinarian, presented following a seizure. Physical examination revealed depression, mild pyrexia (39.1°C) and hypotension (indirect measurement of mean arterial pressure (MAP) 70 mmHg, reference range [rr] 86.6 ± 9.9 mmHg). Bloodwork revealed polycythaemia (packed cell volume [PCV] 0.48 l/l; rr 0.30–0.44 l/l), neutrophilia (7.8 × 103/l; rr 3.0–7.0 × 103/l) and lymphopenia (0.6 × 109/l, rr 1.8–5.0 × 109/l). Cytological examination of a blood smear was not performed. Significant biochemistry profile findings included hypoglycaemia (1.89 mmol/l; rr 4.1–6.5 mmol/l), increased lipase activity (449 u/l, rr less than 39 u/l), increased amylase activity (34 u/l, rr <4 u/l), hypertriglyceridaemia (105 mmol/l, rr 0.15–0.87 mmol/l). Serum sodium, chloride and potassium concentrations were normal but total calcium was abnormally low (2.35 mmol/l; rr 2.80–3.25 mmol/l). Thoracic and abdominal ultrasonography was unremarkable. The clinical signs and laboratory findings were suggestive of acute, severe pancreatitis and septic shock.

Treatment, clinical progression and post mortem findings

Initial treatment consisted of intranasal oxygen (3 l/min), 5% dextrosea (4 mg/kg bwt/min i.v.) and polyionic fluidsb (120 ml/kg bwt/day i.v.). Following resuscitation, a continuous rate infusion of i.v. 0.45% NaCl/2.5% dextrose was administered (200 ml/kg bwt/day). Amikacinc (20 mg/kg bwt i.v. q. 24 h), potassium penicillin Gc (22,000 iu/kg bwt i.v. q. 6 h), metronidazoled (15 mg/kg bwt per os q. 12 h), omeprazolee (4 mg/kg bwt per os q. 24 h), sucralfated (20 mg/kg bwt per os q. 8 h) and flunixin megluminef (0.25 mg/kg bwt i.v. q. 8 h) were administered for treatment and prevention against bacterial translocation, gastrointestinal ulceration and systemic inflammation. Aseptic blood cultures were taken prior to antimicrobial administration and yielded no growth. After resuscitation, the foal became ambulatory but had cortical blindness. Diarrhoea and abdominal distention developed. Faecal Salmonella culture was negative. Assessment for Clostridium spp. toxins and rotavirus was not performed. Abdominal ultrasonography showed peritoneal fluid accumulation and distended, fluid filled small intestine. Abdominocentesis revealed orange, turbid fluid with a normal nucleated cell count, increased protein (42 g/l) and elevated amylase concentration (79 u/l, rr <14 u/l) and lipase concentration (1300 u/l, rr <36 u/l) (Parry and Crisman 1991).

On Day 2, abdominal distention due to worsening peritoneal effusion was relieved by insertion of a drainage catheterg into the peritoneal cavity. Nonfractionated heparin (40 iu/kg bwt subcut. q. 8 h) and soluble insulin (constant rate infusion i.v. 0.25 u/kg bwt/h) were administered after the blood glucose was normalised in an effort to ameliorate hypertriglyceridaemia (8.4 mmol/l, rr 0.15–0.87 mmol/l). On Day 3, serum lipaemia resolved and enteral feeding was resumed. Extrapolating from its use in canines with exocrine pancreatic insufficiency, commercially available pancreatic enzymes were administered (Viokaseh, dose 5 ml/50 kg bwt) to aid appropriate digestion of enteral feedstuffs. Serum amylase, lipase and triglyceride concentrations were within reference intervals by Day 5. Persistent blindness, diarrhoea, and poor appetite resulted in euthanasia of the foal on Day 6. Post mortem examination confirmed severe, subacute to chronic pancreatitis with fibrosis and fibrinous peritonitis as well as ischaemic necrosis of the frontal cortex of the brain.

Case 2

Case history, clinical and laboratory findings

A 5-day-old Appaloosa filly, healthy for the first 4 days of life with IgG >8.0 g/l as measured by the referring veterinarian, presented for diarrhoea of less than 24 h duration. Physical examination identified obtundation, dilated pupils, mild abdominal distension, tachycardia (140 beats/min), tachypnoea (60 breaths/min) and hypotension (MAP = 60 mmHg). Abnormal haemogram findings included polycythaemia (PCV 0.52 l/l; rr 0.30–0.44 l/l), leucopenia (1.9 × 109/l, rr 5.2–10.2 × 109/l), neutropenia (0.7 × 103/l; rr 4.1–9.5 × 103/l) with left shift (0.5 × 109/l, rr 0 /l), mild toxic changes and lymphopenia (0.6 × 109/l, rr 1.0–3.5 × 109/l). Biochemistry abnormalities included hypoglycaemia (2.33 mmol/l; rr 4.1–6.5 mmol/l), pre-renal azotaemia (urine specific gravity: 1.032, rr 1.002–1.008; creatinine: 152.5 µmol/l, rr 68.6–137 µmol/l), hypoalbuminaemia (16 g/l, rr 28–38 g/l), hypoglobulinaemia (12 g/l, rr 24–44 g/l), increased anion gap (26 mmol/l, rr 8–19 mmol/l), increased lipase activity (326 u/l, rr <39 u/l), increased amylase activity (155 u/l, rr <4 u/l), and hypertriglyceridaemia (53.4 mmol/l, rr 0.15–0.87 mmol/l). Venous blood gas analysis revealed metabolic acidosis (pH 7.20, rr 7.32–7.44; bicarbonate 11 mmol/l, rr 24–31 mmol/l); lactate 1.12 mmol/l, rr 0.03–0.17 mmol/l. Abdominal ultrasonography demonstrated anechoic peritoneal fluid, nonmotile small intestine, and an ill-defined hypoechoic mass on midline of the cranial-ventral abdomen. Abdominocentesis yielded an opaque orange chylous effusion with increased protein (56 g/l, rr <25 g/l), nucleated cell count (2.3 × 109/l, rr <1.5 × 109/l), amylase concentration (729 u/l, rr 0–14 u/l), lipase concentration (1746 u/l, rr 0–36 u/l). Triglyceride concentration was 16.7 mmol/l (rr not available). Physical examination, clinical pathology and ultrasonographic findings were consistent with acute severe pancreatitis.

Treatment and post mortem findings

Treatment for presumed septic shock was instituted with intranasal oxygen (3 l/min), 5% dextrosea (4 mg/kg bwt/min i.v.), Hetastarchi (10 ml/kg bwt i.v.) and potassium penicillinc (22,000 iu/kg bwt i.v. q. 6 h). Abdominal pain and seizures developed within 3 h of presentation and the foal was subjected to euthanasia. Necropsy revealed 2 l of fibrinous, opaque abdominal fluid and a 13 × 13 × 6 cm white to tan mass involving the root of the mesentery (Fig 1). The mass was adhered to the peritoneal surface of the left kidney, ileum and caecum near the ileocaecal junction, proximal duodenum and caudal vena cava. Cut surface was white to tan with granular appearance, central necrosis and haemorrhage. There was no evidence of enteritis or infiltration into the intestinal wall. A normal pancreas was not detected. Histologically, the mass was composed of diffusely necrotic pancreatic tissue that was separated by large areas of fibrin and haemorrhage (Fig 2). Surrounding the pancreatic lobules were moderate numbers of degenerative neutrophils. The adjacent mesenteric adipose tissue was extensively necrotic with a peripheral rim of highly degenerative inflammatory cells. Histological findings were consistent with a severe, acute necrotising pancreatitis and peritonitis.

Figure 1.

Case 2. Cranial abdominal mass composed of multiple adhered loops of intestine and white to tan, granular material (necrotic adipose and pancreatic tissue). Black solid arrows surround mass.

Figure 2.

Case 2. a) Necrotic pancreas; note the expansion and replacement of the pancreatic tissue with a loose eosinophilic fibrinous stroma. Haematoxylin and eosin, Bar = 1 mm; b) Necrotic pancreatic tissue characterised by retention of tissue architecture but loss of cellular detail, nuclear pyknosis and karyolysis. Haemotoxylin and eosin. Bar = 100 µm


Severe acute pancreatitis has rarely been documented in equids. In the one report of SAP in a foal (Taintor et al. 2006), inflammatory peritoneal effusion and plasma hyperlipaemia were discovered prior to euthanasia. Pancreatic and peripancreatic fat necrosis with pancreatic vasculitis and fibrinous peritonitis were found at necropsy. Serum collected before euthanasia but submitted after necropsy had mild elevation in lipase activity. The cause of SAP in that foal was not determined.

Specific conditions associated with pancreatitis in dogs and man include: pancreatic duct obstruction, pancreatic ischaemia, abdominal trauma, reflux of duodenal secretions into pancreatic duct, some viral, bacterial, parasitic and protozoal infections (Williams and Steiner 2005), high fat diets (Baker 1978), obesity and hyperlipidaemia (Goodhead 1971). Zinc, calcium (Williams and Steiner 2005) and a variety of drugs have also been associated with acute pancreatitis. Some drugs are thought to cause SAP via increased serum triglyceride concentration while the mechanism of others is unknown (Lindberg 2009). Hyperlipaemia has long been associated with pancreatitis in dogs (Williams and Steiner 2005) and also occurs in 1–4% of human cases of pancreatitis (Lindberg 2009; Tsuang et al. 2009). However, it is unknown if hyperlipaemia is the primary cause or is secondary to pancreatitis. Two reports exist of hyperlipaemia in mature ponies with SAP but the temporal order was unknown (Bulgin and Anderson 1983; Dacre et al. 2003). Previous reports of hyperlipaemia in 2 sick neonatal foals had no clinical evidence of SAP, however pancreatic enzymes were not measured (Hughes et al. 2002; Tan et al. 2005). In man, familial hyperlipidaemias are associated with frequent episodes of pancreatitis that respond to serum triglyceride control and often initially presents during infancy (Tsuang et al. 2009). These predisposing processes cause pancreatic hyperstimulation and/or duct occlusion resulting in co-localisation of inactive digestive enzymes and pancreatic lysosomes, causing intrapancreatic trypsin activation and SAP (Williams and Steiner 2005). In addition, when excessive free fatty acids secondary to hypertriglyceridaemia (Bakos et al. 2008) create an acidic environment (Yang et al. 2009), trypsin inhibitors lose efficacy, resulting in direct pancreatic damage. Genetic polymorphisms in trypsin or its inhibitors may result in premature activation and SAP (Le Maréchal et al. 2004; Keim 2008; Whitcomb 2010).

Severe acute pancreatitis is associated with marked systemic effects, multiple organ failure and, in man, mortality rates of up to 20% (Lilley and Beeman 1983; Lindberg 2009). Spread of pancreatic enzymes and inflammation into the abdomen leads to increased vascular permeability and peritonitis (Lindberg 2009). Some patients later develop chronic pancreatic exocrine enzyme deficiency causing maldigestion, diarrhoea and weight loss. Pancreatic endocrine function can be affected but is less common (Lowenfels and Maisonneuve 2009). Common clinical signs reported in mature horses with SAP have been abdominal pain, gastric reflux and hypovolaemic shock (Bakos et al. 2008). These signs have been reported in horses with acute pancreatitis and no primary intestinal diseases. Many of these signs were found in the 2 cases described and in the previously reported foal (Taintor et al. 2006). All 3 foals with SAP have had visibly lipaemic plasma and orange coloured (probably reflecting the combination of haemorrhage and lipaemia) high protein peritoneal fluid, and signs suggestive of cerebral dysfunction (seizure, coma or cortical blindness). The cause of these signs may be hypoglycaemia or ‘pancreatic encephalopathy’, which occurs in man due to cerebral microthrombosis and infarction (Zhang and Tian 2007).

Laboratory abnormalities associated with SAP include increased activities of serum and peritoneal amylase and lipase (Lilley and Beeman 1983). There are no published reference ranges for amylase and lipase in 5-day-old foals therefore, values were compared with published ranges for healthy 24–48 h Thoroughbred foals (Ricketts et al. 2006), and 4 healthy 5-day-old foals at the Cornell University Equine Park. Gamma glutamyl transferase, although present in the equine pancreas (Ford and Adam 1981), was not increased in these 2 cases nor in the single case report of SAP in a mature donkey (Kawaguchi et al. 2004) and should not be considered a sensitive indicator of equid pancreatic disease. Necropsy findings include swollen, oedematous pancreas with haemorrhage and necrosis. Inflammatory masses such as that described in Case 2, are well documented in man, but rarely found in domestic animals (Charles 2007).

Treatment of SAP should address shock and the underlying condition. There is only one report of successful treatment, which was general and supportive, in the mature horse (Bakos et al. 2008) and no documented cases of treating SAP in the foal. The medical treatment of Case 1, which included specific treatment for hyperlipaemia with heparin and insulin, may have helped in the resolution of the hyperlipaemia, increased pancreatic enzymes and haemodynamic instability but did not prevent the development of pancreatic fibrosis and fibrinous peritonitis. The failure of the diarrhoea to improve with the pancreatic enzyme treatment (Viokase) might have been due to the severe peritonitis in the foal rather than maldigestion of fat and carbohydrates, which was not evaluated by faecal analysis. Unless a cause is proven, future cases may be treated similarly, but low molecular weight heparin may be indicated to alleviate microthrombosis in the pancreas and brain (Jain and Zimmerschied 2009; Lu et al. 2010). Additional efforts should be made to decrease the peritoneal inflammation with abdominal lavage and fibrinolytics. Pentoxifylline may reduce the severity and mortality associated with SAP (Matheus et al. 2009; Abdin et al. 2010).

The cause of SAP in these 2 foals could not be determined. Sepsis, acute enteritis and/or a gastrointestinal strangulation were considered as precipitating factors; however, they were not supported by the necropsy findings. Vasculitis and/or lymphatic obstruction within the pancreas were not supported by necropsy either (Taintor et al. 2006). A genetic basis for the hyperlipaemia in the 2 foals reported here could not be ruled out, as they were the same breed with common distant ancestors; however, familial hyperlipidaemias have not been documented in horses. There were no drugs or supplements administered to these foals prior to presentation. Mammary secretions from the dam of Case 2 were assessed for fat content immediately after the foal died and were found to be within normal range for equine milk fat (2%), ruling out high fat diet as a cause of hyperlipaemia and acute pancreatitis (Doreau et al. 1992). Other maternal factors were inapparent as mare health during gestation and gestation lengths were unremarkable.

Severe acute pancreatitis should be included as a differential for neonatal foals exhibiting acute onset of neurological signs, hypovolaemic shock and abdominal crisis associated with a chylous-haemorrhagic peritonitis, diarrhoea and lipaemic serum. Abnormally high concentrations of serum amylase and lipase in the blood and peritoneal fluid will confirm the diagnosis. Although the cause of SAP in foals is unknown, it appears that foals might be most susceptible within the first 5 days of life.

Conflicts of interest

No conflicts of interest have been declared.

Sources of funding



The authors would like to thank Dr Joe Wakshlag for his nutritional consultation in regards to Case 2.

Manufacturers' addresses

a Hospira Inc, Lake Forest, Illinois, USA.

b Plasmalyte, Baxter Animal Health Corporation, Deerfield, Illinois, USA.

c Pfizer Roering, New York, New York, USA.

d Teva Pharmaceuticals, Sellersville, Pennsylvania, USA.

e Merial Limited, Duluth, Georgia, USA.

f Bulter, Dublin, Ohio, USA.

g Abbott Laboratories, Abbott Park, Illinois, USA.

h Fort Dodge, Fort Dodge, Iowa, USA.

i B. Braun Medical, Inc. Allentown, Pennsylvania, USA.