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EQUINE VETERINARY EDUCATION / AE / NOVEMBER 2020
of full-thickness intestinal necrosis (thickened, dark red, or black intestinal wall) not associated with strangulation of the mesenteric vasculature. Cases of suspected or confirmed focal eosinophilic colitis (Edwards et al. 2000) were excluded. Medical records of all horses diagnosed with NSII were reviewed and details of signalment, history, clinical findings, treatment, and outcomes were recorded. Where available, results of gross post- mortem examination and histopathological examination were documented. If taken during surgery, biopsies were placed immediately into 10% neutral buffered formalin (NBF); post-
mortem samples were collected within 30 min of death and fixed immediately in NBF. The site of sampling was selected by
the clinician, based on the gross surgical or post-mortem findings. Tissues were processed routinely for histology.
Results Fifteen horses with NSII were identified during the study period (Table 1). These included five cobs, four Thoroughbred or Thoroughbred crosses, two Irish sport horses, one New Forest pony, one Trotter, one Warmblood, and one Arabian cross. The age at presentation ranged from 2 to 29 years (mean 16.3 years, median 13 years). There were seven mares, one colt and seven geldings. The horses presented in every season of the year: February (one), March (one), April (two), May (two), June (one), July (two), August (one), September (one), October (two), and December (two). The worming history was recorded for two horses; one had received fenbendazole 6 weeks prior to presentation (Case 8) and the second had a routine anthelmintic treatment the day before presentation (Case 7).
Presenting signs and clinical findings The major presenting clinical signs included: acute colic ≤24 h duration (ninehorses: Cases 2,3,5,6,7, 8,9,12, and 13); diarrhoea, depression, and inappetence (four horses: Cases 1, 4, 11, and 14); and low grade chronic or recurrent colic, depression, and inappetence (two horses: Cases 10 and 15; Table 1). One horse (Case 9) presented with both acute colic and mild diarrhoea (in the absence of depression and inappetence). Tachycardia (heart rate varying from 48 to 120 beats/min) was recorded at presentation in all 14 horses where this was recorded (clinical parameters were not recorded thoroughly in Case 12 because the horse was uncontrollably painful on admission), and tachypnoea (respiratory rate 16–68 breaths/min) in 11/14 (Cases 1, 2, 3, 4, 8, 9, 10, 11, 13, 14, and 15). Pyrexia (rectal temperature varying from 38.7 to 39.8°C) was recorded in 8/14 (Cases 1, 4, 5, 10, 11, 13, 14, and 15; rectal temperature not recorded in Case 12), including all four horses presenting with diarrhoea and both horses presenting with chronic/recurrent colic. Borborygmi were reduced or absent at presentation in 12/14 (Cases 1, 2, 3, 4, 5, 6, 7, 8, 10, 11, 13, and 15), including 7/9 horses with acute colic, 3/2 horses with chronic/recurrent colic and 2/4 horses with diarrhoea. The mucous membranes were congested/toxic in appearance in 5/14 horses (Cases 1, 4, 10, 11, and 13), pale in 3/14 (Cases 3, 7, and 8), and cyanotic in 1/14 (Case 5); the capillary refill time was prolonged (>2s) in 8/14 horses (Cases 1, 2, 3, 5, 7, 10, 11, and 13). Thirteen of the 15 horses had a rectal examination
performed, and abnormal findings were found in 10: six had gas distended large intestine, (Cases 2, 3, 5, and 12 which presented with acute colic, Case 13 which presented with
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chronic/recurrent colic, and Case 4 which presented with diarrhoea); one also had a large intestinal impaction (Case 5), and four had distended small intestine (Cases 6, 7, 8 which presented with acute colic and Case 10 which presented with chronic/recurrent colic). No palpable abnormalities of the mesenteric root were detected in any horse. Abdominocentesis was performed at admission in 7/15 cases; peritoneal fluid was serosanguinous in 3/7 (Cases 2, 8, and 5 which presented with acute colic) and turbid in 4/7 (Cases 10 and 15 which presented with chronic/recurrent colic, and Cases 1 and 14 which presented with diarrhoea) with total nucleated cell counts ranging from 1.2 9 109/l to >400 9 109/l (rr < 5 9 109/L). Cytological examination of peritoneal fluid showed a neutrophilic exudate in the four horses with turbid peritoneal fluid (Cases 1, 10, 14, and 15). Trans-abdominal ultrasonography was performed in 9/15 horses (GE Logiq E9 or GE Logiq P5 ultrasound scanners) and
clinically significant abnormalities were found in 7/9, including fluid-filled large intestine in 2/7 (Cases 4 and 11 which presented with diarrhoea) with increased large intestine mural thickness in 1/7 (Case 11), immotile distended small intestine in 5/7 (Cases 5 and 8 which presented with acute colic, Cases 10 and 13 which presented with chronic/ recurrent colic, and Case 1 which presented with diarrhoea,) and increased volume of free peritoneal fluid in 2/7 (Cases 5 and 10).
Routine haematology and serum biochemistry were
performed at admission in 14/15 horses. Seven horses were haemoconcentrated (PCV 49.7–68%; rr 32–46%) (Case 5 which presented with acute colic, Cases 10 and 13 which presented with chronic/recurrent colic, and Cases 1, 4, 11, and 14 which presented with diarrhoea). Three horses were leucopaenic (WBC count 1.6 9 109/L to 4.0 9 109/L; rr 5– 10 9 109/L) (Case 5 which presented with acute colic, Case 10 which presented with chronic/recurrent colic, and Case 4 which presented with diarrhoea) and three had a leucocytosis with neutrophilia (Case 2 which presented with acute colic, Case 15 which presented with chronic/recurrent colic, and Case 1 which presented with diarrhoea). Two horses were hypoproteinaemic (48 and 44 g/L) (Case 4 which presented with diarrhoea and Case 7 which presented with acute colic) and two were hyperproteinaemic (79 and 80 g/ L) (Case 5 which presented with acute colic and Case 14 which presented with diarrhoea), (rr 58–75g/L). One horse was hypoalbuminaemic (21 g/L) (rr 28–35 g/L) (Case 7 which presented with acute colic). Other abnormalities recorded included elevated serum activities of gamma glutamyl transferase (2/14), alkaline phosphatase (1/14), lactate dehydrogenase (3/14), glutamate dehydrogenase (2/14), aspartate transferase (3/14), creatinine kinase (6/14), and urea (4/14). Serum amyloid A was measured in five horses and was elevated in all (11.03–5240 mg/L; rr < 10 mg/L) (Cases 2 and 6 which presented with acute colic, Cases 10 and 15 which presented with chronic/recurrent colic, and Case 4 which presented with diarrhoea). Fibrinogen was measured in six horses and 4/6 had hyperfibrinogenaemia (4.4–8.1 g/L; rr < 4 g/L) (Case 2 which presented with acute colic, Cases 10 and 15 which presented with chronic/ recurrent colic and Case 14 which presented with diarrhoea). Faecal salmonella cultures and clostridium PCR were performed in 3/5 horses with diarrhoea and were negative in all cases. A faecal worm egg count was performed in 3/15 horses and was negative in two and had a count of 175
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