Case Report Nonstrangulating Small Colon Obstruction Caused by a Submucosal Haematoma S
Total Page：16
File Type：pdf, Size：1020Kb
EQUINE VETERINARY EDUCATION / AE / APRIL 2006 89 Case Report Nonstrangulating small colon obstruction caused by a submucosal haematoma S. STAHEL*, C. B. RILEY, M. WICHTEL AND P.-Y. DAOUST† Departments of Health Management and †Pathology and Microbiology, Atlantic Veterinary College, University of Prince Edward Island, 550 University Avenue, Charlottetown, Prince Edward Island C1A 4P3, Canada. Keywords: horse; colic; small colon; haematoma; submucosa Introduction This report describes a case of nonstrangulating obstruction resulting from a submucosal haematoma of Compared with other intestinal causes of equine colic, the small colon in a horse. disorders of the small colon are relatively uncommon (White 1990; Edwards 1992). One review of specific intestinal Case details disorders reported the prevalence of small colon and rectal diseases to be between 2.9 and 17.7% (Keller and Horney History 1985). More recent estimates reported a 3.5% incidence in all admitted cases (White 1990) to 4.2% incidence in horses An 11-year-old Morgan gelding was presented to the Atlantic undergoing celiotomy for colic (Edwards 1992). American Veterinary College Veterinary Teaching Hospital (VTH) with a miniature horses, Arabians and ponies are reported to be the 36 h history of colic. The gelding was administered anthelmintic breeds at greatest risk of developing small colon disorders drugs and vaccinated every 3 months; anthelmintics (pyrantel (Ragle et al. 1992; Edwards 1997). pamoate ~13 mg/kg bwt per os) had been given 38 days prior Submucosal haematomas of the small colon are to admission, and vaccination against rhinopneumonitis/herpes uncommon, with only a few cases having been reported in myeloencephalopathy (EHV-1 and -4), tetanus, equine influenza the last 20 years (Pearson and Waterman 1986; Dart et al. (types A1 and A2) and rabies 11 weeks prior to admission. 1992; Edwards 1992). Earlier reports found small colon Faecal output had initially been reduced and was absent haematomas in 0.4–2.4% of horses that underwent for 18 h prior to presentation. The horse’s heart rate did not celiotomy due to colic (Pearson et al. 1975; Speirs et al. exceed 48 beats/min over the 36 h period. A nasogastric tube 1981), and in 0.2% of horses examined for colic (Huskamp was placed twice by the referring veterinarian during the 1982). One author reported a 0.67% prevalence of small course of the disease and failed to yield reflux. Flunixin colon haematomas in horses referred for colic surgery meglumine administered 3 times at 1.1 mg/kg bwt by the (Edwards 1992), but more recent retrospective and referring veterinarian, resulted in temporary analgesia; prospective studies have not reported cases of small colon however, the horse became uncomfortable again 8–9 h after haematomas within their study populations (Hillyer et al. each dose. No abnormal findings were identified on rectal 2002; Proudman et al. 2002). Affected horses in recent examination by the referring clinician at first visit. A second reports were, on average, 14 years of age (range 8–23 years; rectal examination 24 h later resulted in a tentative diagnosis n = 7; age not documented in 4 cases) (Pearson and of pelvic flexure impaction. The horse was subsequently Waterman 1986; Dart et al. 1992; Edwards 1992). No gender referred to the VTH. or breed predisposition has been identified and the lesion has not been described previously in foals (Pearson et al. 1975; Clinical examination Speirs et al. 1981; Pearson and Waterman 1986; Adams et al. 1988; Dart et al. 1992; Edwards 1992; Vatistas et al. 1996; Upon presentation to the VTH, the horse was quiet and Cable et al. 1997). Haematomas of the equine depressed. Dehydration was estimated to be ~5% gastrointestinal tract have also been reported in the jejunum (determined by skin tenting) and borborygmi were reduced (Kobluk and Smith 1988; Jach and Allmeling 1990; Kopf in volume and infrequent, especially on the left side of the 1990) and mesentery (van Hoogmoed and Snyder 1996). abdomen. Rectal temperature and respiratory rate were 36.8°C and 12 breaths/min, respectively. Heart rate was *Author to whom correspondence should be addressed. 44 beats/min. The horse’s mucous membranes were pink, 90 EQUINE VETERINARY EDUCATION / AE / APRIL 2006 M Fig 1: Intramural haematoma of the small colon. The haematoma is obstructing the whole intestinal lumen, making it impossible for faeces to pass through. Fig 2: Circular muscle layer and submucosa of the small colon. There is marked infiltration of inflammatory cells into the with capillary refill time <2 secs. On rectal examination, the muscle layer (M) and haemorrhage in the submucosa (top right pelvic flexure was impacted with ingesta. No other corner). H&E; bar = 100 µm. abnormalities were identified. Scant, dark and dry faeces were removed from the rectum. Abdominocentesis failed to Post mortem findings produce fluid. Haematology revealed an inflammatory leucogram characterised by a normal total leucocyte count Necropsy was performed 12 h following euthanasia. On gross (7.3 x 109/l; reference range [rr] 5.5–12.5 x 109/l), left shift examination, a haemorrhagic and congested area was found in (bands 0.36 x 109/l) and 1+ toxic change. Fibrinogen level the small colon 2 m proximal to the anus. On palpation, the was 4 g/l. Serum biochemistry analysis revealed a contents of the described area had a gelatinous consistency. A hypokalaemia (2.5 mmol/l; rr 3.0–5.0 mmol/l), large intramural haematoma, obstructing the entire small hypophosphataemia (0.82 mmol/l; rr 1.0–1.8 mmol/l), colonic lumen, was diagnosed on section (Fig 1). The hypomagnesaemia (0.64 mmol/l; rr 0.74–1.02 mmol/l), haematoma was approximately 17 cm long, 8 cm in diameter, hyperglycaemia (7.6 mmol/l; rr 3.6–5.6 mmol/l) and soft and poorly organised. Proximal to the obstruction, the γ elevated -glutamyltransferase (GGT) (40 u/l; rr 0–25 u/l). small colon was filled with firm faecal balls. The large colon was With the exception of the elevated GGT, those distended with a greater amount of soft ingesta than would be abnormalities were thought to be due to reduced dietary expected in a normal horse subjected to euthanasia. The intake and stress. Cholestasis was suspected based on the caecum and right dorsal colon were gas-distended. An 8 cm elevation of GGT in the presence of a normal sorbitol long portion of the mesocolon, adjacent to the small colon and dehydrogenase concentration. immediately proximal to the haematoma, was haemorrhagic. The affected segment of bowel and mesocolon was fixed in Treatment 10% formalin. Sections, 5 µm thick, were cut and stained with haematoxylin and eosin. Histology revealed extensive Lactated Ringer’s solution was administered through a haemorrhage in the mesocolon that extended into the 14 gauge catheter into the left jugular vein. The flow rate was submucosa of the small colon. Inflammatory cells (50% adjusted to replace the horse’s fluid deficit of 5% within 12 h. Following rehydration the rate of fluid administration neutrophils and 50% mononuclear leucocytes), fibrin, was reduced to 90 ml/kg bwt/day. Analgesia was provided fibroblasts and new capillaries had infiltrated the tissues (flunixin meglumine 1.1 mg/kg bwt i.v. q. 24 h) and food (mesocolon, colonic circular and longitudinal muscle layers, and withheld. Over the next 36 h, the horse’s condition submucosa) within and at the periphery of the large areas of deteriorated. The painful episodes increased, response to clotted blood (Fig 2). Neovascularisation and fibroblasts were analgesic medication decreased and the heart rate prominent in the mesocolon, suggesting that the process was intermittently rose to 72 beats/min. No faeces had passed subacute (>5 days’ duration). Within the mesocolon there was since admission and borborygmi were still reduced in volume also necrosis and haemorrhage in the walls of a few small blood and infrequent. Findings on rectal examination at this time vessels. The vascular lesion was not associated with perivascular were supportive of a tentative diagnosis of large colon necrosis or haemorrhage. A portion of the intestinal mucosa at displacement. Passage of a nasogastric tube was attempted, the level of the haematoma had sloughed off, leaving only a but the tube could not be advanced into the stomach. Based thin layer of bacteria covering the submucosal surface. on the poor response to therapy, surgical exploration was The final post mortem diagnosis was focal, subacute recommended. The horse’s owner opted to subject the horse submucosal haematoma of the small colon with secondary to euthanasia. luminal obstruction. 92 EQUINE VETERINARY EDUCATION / AE / APRIL 2006 Discussion resulting in clinical signs. It is possible that the initial injury occured in the mesocolon (chronic changes were most Small colon haematomas have only been reported previously in prominent there) and that the colonic wall was secondarily mature horses (Pearson and Waterman 1986; Dart et al. 1992; affected. Gross findings suggested a localised disease process. Edwards 1992). Although foals may suffer from small colon However, histological evaluation of other grossly normal obstruction (Adams et al. 1988), submucosal haematomas sections of both small and large intestines should have been have not been described. This may suggest that small colon performed to rule out multifocal disease. submucosal haematomas are neither congenital nor In most reported cases of equine small colon haematomas, developmental, but rather that they are an acquired condition. the cause remains speculative. Equine strongyle disease has The duration of colic in horses with submucosal been postulated as a possible cause (Keller and Horney 1985). haematoma of the small colon reported in the history varies The larvae as well as the adult gastrointestinal nematodes may from 6 h to 5 days (Speirs et al.