EQUINE VETERINARY EDUCATION / AE / NOVEMBER 2020
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TABLE 2: Pathological findings Case no.
1 2 3 4
Gross lesions (surgical and/or post-mortem)
Peritonitis. Multifocal regions of full thickness necrosis of jejunum 10– 15 cm long. Typhlocolitis.
Focal 75 cm long area of necrosis at pelvic flexure with multiple mesenteric adhesions.
Multifocal areas of jejunal necrosis distant to anastomosis site.
Excess peritoneal fluid. Typhlocolitis. Multifocal areas of necrosis in jejunum.
5 6 7
8 9
10
Focal area of necrosis left ventral colon adjacent to mesenteric attachment 45 cm long. Peritonitis.
Severe fibrinous peritonitis. Enteritis and typhlocolitis. Multifocal areas of jejunal necrosis.
Peritonitis. Focal necrosis of mid jejunum. Necrosis of ileal stump.
Multifocal areas of necrosis of jejunum.
Focal necrosis of pelvic flexure and left dorsal colon. Diffuse colitis.
Necrosis 10 distal jejunum with focal rupture and peritonitis.
Intestinal vascular thrombosis and infarction.
Full thickness jejunal coagulative necrosis with fibrin thrombi within the remnants of submucosal vessels. Severe acute and chronic inflammation of the mesentery with multifocal necrosis and haemorrhage.
11 12 13 14 15
Diffuse colitis. Multifocal areas of necrosis of jejunum, ileum, caecum, and large colon.
Caecal apex necrosis.
Multifocal areas of necrosis of distal jejunum, ileum, caecum, and mesentery. Diffuse peritonitis.
Celiotomy wound breakdown. Focal area of necrosis of left dorsal colon. Typhlocolitis.
Extensive necrosis of left ventral colon with extensive adhesions of necrotic colon to body wall and spleen.
Intestinal vascular thrombosis and infarction
Transmural coagulative necrosis of small intestinal and caecal walls with numerous thrombosed vessels.
Thrombosis and ischemic necrosis of left dorsal colon wall, with vasculitis and fibrinous necrosis of jejunum.
Transmural coagulative necrosis of colon wall with numerous small thrombosed vessels. Necrosis and haemorrhage of mesentery with thrombosed vessels.
were acute colic (60% of cases), chronic/recurrent colic with depression (13%) and diarrhoea with depression (27%), consistent with the underlying pathological processes. The horses presenting with diarrhoea all had associated colitis or typhlocolitis, which was the likely underlying predisposing factor to developing NSII in those animals. Common clinical and laboratory findings also reflected the underlying intestinal damage and subsequent shock, including tachycardia, pyrexia, tachypnoea, prolonged capillary refill time, haemoconcentration, leucopenia or leucocytosis, and turbid peritoneal fluid due to peritonitis. Interestingly the clinical presentations of the horses with S. vulgaris associated NSII described by Pihl et al. (2018) were somewhat different to the
Full-thickness coagulative necrosis of jejunum. Fibrinous peritonitis. Enteritis.
Focal full-thickness jejunal necrosis and vascular thrombosis.
Histopathological findings
Full-thickness coagulative necrosis of jejunum.
Extensive haemorrhage and necrosis of colon wall at pelvic flexure. Thrombosis of submucosal vessels.
Focal full-thickness jejunal necrosis, haemorrhage, and vascular thrombosis. Fibrinocellular peritonitis.
Extensive jejunal mucosal necrosis with coagulative necrosis of the submucosa, and patchy necrosis of the outer muscular layers and serosa. Necrotising typhlocolitis.
Aetiopathogenesis Typhlocolitis
Unknown
Initial strangulating small intestinal obstruction
Colitis
Unknown
Initial strangulating small intestinal obstruction
Initial strangulating small intestinal obstruction
Unknown Colitis
Unknown
Colitis Unknown Unknown Colitis Unknown
majority of our cases, being characterised most commonly by depression and anorexia, with either no or only mild colic, and no signs of shock (although all of the horses had a history of colic prior to admission to the hospital); only two horses in this study presented with low grade chronic/recurrent colic, depression, and inappetence that could be considered similar to the typical presentation described by Pihl et al. (2018). The reason for this apparent difference in presentation is unclear, but likely relates to the different aetiopathogenesis of the NSII in the two groups of horses. Similar to the horses with NSII described by Pihl et al.
(2018), all horses in this study had at least one intestinal infarction and some had several. Infarctions were located in
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