The periparturient mare: when gut attacks

The entirety of the intestinal tract cannot be palpated or imaged making evaluation of the periparturient foaling mare difficult.  Response to nasogastric intubation, clinical impression and evaluation of blood work therefore become important aids to diagnosis.  Ultrasonographic findings may not point towards any particular lesion and the majority of the intestinal tract is not visible in the pregnant mare, however if seen changes in gut location, anatomy or size may be the only clue of developing problems.  Regrettably, the only indication of intestinal compromise or rupture may be the rapid onset of fulminant peritonitis and signs of endotoxemia.  Any compromise to the gastrointestinal tract, promoting translocation of bacteria and inflammatory mediator production, or more seriously direct spillage of intestinal content or feces such as with rectal laceration, results in the onset of endotoxemia.  Fever, depression, and profound circulatory disturbances result.  Concurrently, pain results directly from intestinal compromise and peritonitis.  Then it is most often too late.

The large colon is at increased risk of displacement of torsion in postpartum mares.1  In one review this was the most common diagnosis for referral emergency presentations of postpartum mares.2  Chronic cases may have vague presenting signs including inappetence and depression.3  Ultrasonographic evaluation reveals increased wall thickness, gaseous distension and loss of sacculations.4  The cecal and colonic mesenteric vessels usually present in the right paralumbar fossa coursing ventrally become engorged and tortuous.5, 6  Colonic impaction may result from diminished water intake, depressed motility due to systemic disease and inappetence, NSAID-related motility decrease, and pain resulting from perineal trauma slowing fecal passage.  

The most common site of cecal rupture is the apex.7  Fetal hoof compressing tympanic cecal wall is thought to cause pressure necrosis and rupture.8  Non-steroidal anti-inflammatory drugs used for post foaling discomfort may reduce cecal motility promoting gas distension, further stressing already devitalized tissue.

Small colon may suffer bruising from compression during foaling.  The small colon has a relatively short mesocolon which can tear with passage of the fetus disrupting vasculature.7, 9  Entrapment of small colon within these rents may cause segmental necrosis.9  Lesser trauma may result in impaction and colic with variable signs of systemic disease.  Increased peritoneal fluid with inflammatory changes in conjunction with increasing signs of endotoxemia may be the first indication of small colon devitalization.

Small intestinal strangulation can be suspected when distension, mural thickening and loss of motility are noted.10  Jejunum may become incarcerated through a tear in the mesentery.11  Dilated small intestine with motility has been associated with large colon lesions, whereas wall thickening with motility suggests peritonitis.10  As with small colon, disruption of the blood supply may cause varying degrees of necrosis to ensue.

Multiple regions of viscera can be simultaneously entrapped.  Diaphragmatic hernia, a rare parturient complication with a guarded prognosis, has been reported to entrap small intestine, large intestine, stomach, spleen and liver.12, 13  With ultrasonography, strangulated gut may appear cranial to the diaphragm, acoustic shadowing the lung may be present, and increased pleural fluid and peritoneal fluid is likely.  Intermittent entrapment of viscera can make diagnosis difficult during periods without overt pain.

Non-surgical conditions such as enteritis or enterocolitis may result from altered feed intake and quality, or the addition of medications (e.g. placentitis treatment, post foaling conditions).  Pain from intestinal inflammation and distension due to both diminished gastrointestinal transit and increased gas production may be as severe as surgical lesions.

So many problems, so next time we’ll talk about something good.  Colostrum – nature’s miracle.

 

1.    Hance SR and Embertson RM. Colopexy in broodmares: 44 cases (1986-1990). J Am Vet Med Assoc 1992;201:782-787.

2.    Dolente BA, Sullivan EK, Boston R et al. Mares admitted to a referral hospital for postpartum emergencies: 163 cases (1992-2002). J Vet Emer Critic Care 2005;15:193-200.

3.    Doyle AJ, Freeman DE, Sauberli DS et al. Clinical signs and treatment of chronic uterine torsion in two mares. J Am Vet Med Assoc 2002;220:349-353.

4.    Abutarbush SM. Use of ultrasonography to diagnose large colon volvulus in horses. J Am Vet Med Assoc 2006;228:409-413.

5.    Grenager NS and Durham MG. Ultrasonographic evidence of colonic mesenteric vessels as an indicator of right dorsal displacement of the large colon in 13 horses. Equine Vet J 2011;43:153-155.

6.    Ness SAL, Bain FT, Zantingh AJ et al. Ultrasonographic visualization of colonic mesenteric vasculature as an indicator of large colon right dorsal displacement or 180° volvulus (or both) in horses. Can Vet J 2012;53:378-.

7.    Frazer GS. Post partum complications in the mare. Part 2: Fetal membrane retention and conditions of the gastrointestinal tract, bladder and vagina. Equine Vet Educ 2003;15:91-100.

8.    Platt H. Caecal rupture in parturient mares. J Comp Path 1983;93:343-346.

9.    Dart AJ, Pascoe JR, Snyder JR. Mesenteric tears of the descending (small) colon as a postpartum complication in two mares. J Am Vet Med Assoc 1991;199:1612-1615.

10. Klohnen A, Vachon AM, Fischer AT. Use of diagnostic ultrasonography in horses with signs of acute abdominal pain. J Am Vet Med Assoc 1996;209:1597-1601.

11. Gayle JM, Blikslager AT, Bowman KF. Mesenteric rents as a source of small intestinal strangulation in horses: 15 cases (1990-1997). J Am Vet Med Assoc 2000;216:1446-1449.

12. Romero AE and Rodgerson DH. Diaphragmatic herniation in the horse: 31 cases from 2001-2006. Can Vet J 2010;51:1247-1250.

13. Moll HD, Wallace MA, Sysel A et al. Large colon strangulation due to a diaphragmatic hernia in a mare: A case report. J Equine Vet Sci 1999;19:58-59.

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