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EQUINE VETERINARY EDUCATION / AE / OCTOBER 2014


the swelling. Antibiotic impregnated gauze (Kerlix AMD)11 was packed into the defect to keep the incision open and facilitate further drainage. The following day (5 days post operative), the filly


appeared lethargic and mildly tachypnoeic with a temperature 39.4°C. Routine haematology revealed leucocytosis (21.7 × 109/l, rr 5.5–12.5 × 109/l) due to a mature neutrophilia (19.5 × 109/l, rr 3.0–7.0 × 109/l). Abdominal ultrasound was unremarkable showing that the repaired body wall was still intact with motile, nondistended small intestine seen within the abdominal cavity. Thoracic ultrasound revealed mild comet tailing of the cranioventral lung fields bilaterally indicating irregularities in the pleural surfaces. Based on the filly’s clinical signs and thoracic ultrasound findings, a diagnosis of mild pneumonia was made. The filly was started on ceftiofur (Naxcel)12 at 5 mg/kg bwt i.m. once daily. The following day the filly appeared brighter and was


afebrile. The seroma had begun to reform dorsal to the surgical incision so the packing was removed, drainage re-established and the space repacked. Two days later (post operative Day 7) the packing was removed and there was no evidence of the seroma reforming. Repeat haematology showed that the filly’s white blood cell count had returned to the normal reference range (7.3 × 109/l) and she remained bright, alert and afebrile until discharge. The filly was discharged 10 days post operatively with an elastic abdominal bandage in place and prescribed 4 more days of i.m. ceftiofur (5 mg/kg bwt i.m. once daily) to be administered by the owner at home. Stall rest was recommended for an additional 2 weeks followed by 2 weeks in a stall with a small paddock attached.


Outcome A follow-up examination at Littleton Equine Medical Center was performed 4 months after surgery. At this time, there was no observable or palpable defect in the abdominal body wall and ultrasound examination showed no difference in thickness of the overlying abdominal musculature (Fig 5).


Discussion


Congenital abdominal wall defects are thought to occur in utero due to aberrant embryogenesis. In man, intraembryonic mesoderm forms 4 folds around the fourth week of development. The 2 lateral folds bend towards the ventral midline leading to the formation of the lateral and ventral abdominal walls (Mortellaro et al. 2011). Failure of the lateral folds to properly migrate has been linked to defects in closure of the ventral body wall resulting in the more commonly recognised ventral body wall defects (Brewer and Williams 2004). Yet, the pathogenesis of lateral body wall defects remains poorly understood. The defect identified in this case most closely resembles


what has been described as a congenital subcostal hernia in the human literature. In the few cases describing this phenomenon (Nicksa et al. 2009; Raghu et al. 2013) all but one were associated with concurrent developmental abnormalities such as skeletal anomalies and renal malformation. In the one case in which the subcostal hernia was the only abnormality identified, the authors hypothesised that it was probably due to a localised vascular event occurring later in development (Raghu et al. 2013). The filly described in this report had no evidence of any concurrent


© 2014 EVJ Ltd


Fig 5: Follow-up ultrasound performed 4 months after surgery. The body wall (arrowheads) appears intact at the previous surgical site with no visible defects in the overlying musculature.


congenital abnormalities and thus it is possible that her defect was also the consequence of a vascular event that occurred in utero. The hernia in this case was nonreducible, and therefore,


surgical correction was necessary to prevent strangulation of the small intestine. Foals with reducible umbilical hernias <5 cm in diameter have been frequently shown to resolve spontaneously within the first 4 months of life (Enzerink et al. 2000) – thus surgery is often delayed. However, it is recommended that nonreducible or hernias >10 cm in diameter be corrected surgically because the risk of strangulation is high (Kummer and Stick 2012). The decision to close the abdominal wall defect without


the use of a mesh implant was made due to the small size of the hernia and the ability to get complete apposition of the edges without excessive tension. While the current recommendations in human medicine for abdominal wall hernia repair is to use a mesh implant (Luijendijk et al. 2000; Burger et al. 2004), the equine literature is more variable. The size of the defect, body weight of the horse and whether or not the body wall edges can be opposed without excessive tension have historically dictated whether prosthetic mesh implants were used. Previous reports state that if the hernia is >10 cm or the horse >450 kg bwt, then a prosthetic mesh implant is recommended (Tulleners and Fretz 1983; Elce et al. 2005). Yet more recently, Whitfield-Cargile et al. (2011) examined 47 mature horses that had undergone hernia repairs using either primary apposition or a mesh implant and concluded that primary apposition resulted in a good cosmetic outcome and avoided the complications associated with mesh implants. Likewise, Cook et al. (1996) looked at ventral midline incisional hernia repairs and found that the combination of opening the hernia sac followed by primary closure resulted in good long-term outcomes. In this case, the formation of a subcutaneous seroma following surgery was considered a minor complication.


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