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EQUINE VETERINARY EDUCATION / AE / NOVEMBER 2020


TABLE 1: Continued Case no. Age years Breed


13 14 24 19


Sex


Clinical features at presentation


New Forest G Acute colic unresponsive to analgesics.


WB


G Acute diarrhoea (grain overload). Depression and inappetence.


15 13 TbX


G 4-day history of depression, inappetence, and intermittent colic.


Case progression (medical vs. surgical treatment)


Exploratory celiotomy – multifocal areas of necrosis of distal jejunum, ileum, caecum, and mesentery.


Deteriorated despite medical therapy – increasing pain.Exploratory celiotomy – focal area of necrotic left dorsal colon. Resection of necrotic area of colon wall.


Medical treatment. Developed severe unresponsive colic after 24 h. Exploratory celiotomy – extensive necrosis of left ventral colon and extensive adhesions to body wall and spleen.


eggs per gram in one. A larval culture was performed in one case that was negative.


Treatments and outcomes Eleven of the 15 horses underwent exploratory celiotomy due to severe or worsening colic signs and/or peritonitis non- responsive to medical therapy (Cases 2, 3, 5, 6, 7, 8, 10, 12, 13, 14, and 15; Table 1). This included 8/9 horses that presented with acute colic (excluding Case 9 which presented with acute colic and diarrhoea), 2/2 horses that presented with chronic/recurrent colic, and 1/4 horses that presented with diarrhoea. Five of the horses that underwent exploratory celiotomy (Cases 2, 5, 10, 13, and 15) were euthanised at the time of surgery due to the presence of NSII with or without associated peritonitis and intra-abdominal adhesions; the prognosis for these horses was considered to be poor or hopeless, and euthanasia was carried out following discussion with the owners. A further two horses (Case 8 which presented with acute colic and Case 14 which presented with diarrhoea) underwent resection of the affected regions of intestine but the horses were euthanised post-operatively (due to persistent pain in Case 8 and incisional dehiscence of all layers in Case 14). One horse (Case 12) underwent exploratory celiotomy where necrosis of the caecal apex was identified; the affected region was resected and the horse made an uneventful recovery. Three horses that presented with acute colic (Cases 3, 6, and 7) underwent exploratory celiotomy at which time strangulating small intestinal obstructions were diagnosed and treated. All three of these horses developed post-operative reflux and pain, and underwent a repeat exploratory celiotomy where NSII was diagnosed at sites distant to the original strangulating obstruction; two were euthanised at the second surgery and one horse (Case 6) had the affected segment of jejunum resected but deteriorated post operatively and was euthanised. Four horses (Cases 1, 4, and 11 that presented with


diarrhoea, and Case 9 that presented with acute colic and diarrhoea) were managed medically, but either died or were euthanised due to progressive clinical deterioration and development of severe pain, or (in Case 9) development of neurological signs associated with hyperammonaemia; NSII was confirmed in all four horses by post-mortem examination.


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Outcome


Euthanised at surgery.


Euthanised 6 days post-operatively (incisional dehiscence)


Euthanised at surgery.


Pathological findings Gross lesions compatible with NSII (clearly demarcated areas of red/black discolouration and thickening of bowel wall not associated with any evidence of strangulation) were identified either at exploratory laparotomy or at post- mortem examination in all horses (Table 2). Necropsy examination was performed in all 14 horses that died. Lesions compatible with NSII were found in both the small intestine and large intestine. In 9/15 cases there was a single lesion, whereas 6/15 had multiple lesions. Ten horses had lesions in the jejunum, two in the ileum, three in the caecum, and seven in the ascending colon (Figs 1 and 2). Only the small intestine had NSII lesions in seven horses, only the large intestine in six, and both the small and large intestines were affected in two.


Colitis or typhlocolitis was present in six horses, including the five horses that initially presented with diarrhoea (Cases 1, 4, 9, 11, and 14) and one horse (Case 6) which presented with acute colic due to entrapment of jejunum in the epiploic foramen and which had evidence of enteritis at post- mortem examination. No lesions of verminous arteritis were identified in the cranial mesenteric artery or its branches in any case. No renal or non-intestinal infarcts were identified. Results of the histopathological examination of the


affected areas of intestine were recorded in 12 horses. These showed evidence of full-thickness intestinal wall necrosis and thrombosis of intestinal and mesenteric blood vessels (Table 2, Figs 3 and 4).


Discussion


Intestinal ischaemia and necrosis resulting from NSII lead to signs of ileus, peritonitis, and endotoxaemia (White 1981; Hackett 2002). The intestinal necrosis compromises the function of the mucosa, allowing leakage of protein rich fluid, bacteria, and endotoxins across the intestinal wall into the peritoneal cavity and intravascular space. Intestinal spasm causes distension of the proximal intestine with gas and fluid (White 1981; Hardy 2008). These events present clinically as colic and signs of compromised cardiovascular status associated with endotoxaemia and peritonitis. In addition to, or preceding these signs, clinical signs associated with the underlying/predisposing disease process may be evident. Overall, the major presenting clinical signs in the 15 horses


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