Case Report an Unusual Cause of Colic in a Neonatal Foal H

334 EQUINE VETERINARY EDUCATION / AE / JULY 2012

Case Report An unusual cause of colic in a neonatal foal H. Tapio*, M. Hewetson and H.-K. Sihvo Veterinary Teaching Hospital, University of Helsinki, Finland.

Keywords: horse; foal; colic; hernia; diaphragm; congenital

Summary largely upon the age of the animal. Common causes of abdominal pain in the neonatal foal include meconium A case of a neonatal foal with acute colic and respiratory impaction, small intestinal volvulus, enterocolitis, distress is described. The foal presented with signs of acute uroperitoneum, intussusception, herniation and ileus colic and was treated medically. The foal did not respond secondary to other problems such as prematurity, to treatment and 2 h after admission the foal began to neonatal encephalopathy or septicaemia (Bernard 2004; demonstrate signs of respiratory distress. Thoracic and Barton 2006). abdominal radiographs were obtained and a diagnosis of Diaphragmatic hernia is an uncommon cause of acute a diaphragmatic hernia was made. Surgical repair of the abdominal pain in neonatal foals, but should be hernia was recommended but the owner declined and the considered as differential diagnosis, especially if it is foal was subjected to euthanasia. Post mortem findings associated with concurrent respiratory distress. confirmed the diagnosis and revealed that the defect was of congenital origin. Congenital diaphragmatic hernia is Case details an unusual cause of colic in a neonatal foal. History Introduction An 18-h-old Finnhorse colt weighing 49 kg was presented Diaphragmatic hernias rarely occur in horses (Edwards at the University of Helsinki Veterinary Teaching Hospital for 1993; Santschi et al. 1997). Both acquired and congenital acute colic. Pregnancy was full term and the foal had hernias have been reported (Speirs and Reynolds 1976; been delivered without assistance. The foal had needed Collobert et al. 1988; Proudman and Edwards 1992; assistance to stand, however, and did not suckle normally Roelvink et al. 1993; Cheetham 1998; Dabareiner and for at least 3 h after the birth. Approximately 6 h after birth, White 1999); however, the majority of cases are acquired the foal started to demonstrate signs of abdominal pain and traumatic in origin (Santschi et al. 1997). There are only and was treated by the referring veterinarian with flunixin a few reports of congenital diaphragmatic hernias in foals meglumine 1.1 mg/kg bwt i.v. and a phosphate enema. (Collobert et al. 1988; Cheetham 1998). The foal passed some meconium following the enema, but Clinical signs typical of diaphragmatic hernias include continued to demonstrate signs of colic and was referred colic, respiratory distress and exercise intolerance (Speirs to the teaching hospital for further investigation and and Reynolds 1976; Collobert et al. 1988; Proudman and treatment. Edwards 1992; Edwards 1993; Santschi et al. 1997; Branson and Kramer 2000). The severity of the clinical signs depends Clinical findings upon the portion and amount of viscera herniated and whether there are disturbances in blood flow to the On presentation, the foal was able to stand and walk by herniated organs (Edwards 1993). himself but was weak and demonstrating signs of This report describes the clinical presentation and post abdominal pain. The foal was restless and tried to roll. The mortem findings of a neonatal foal with a congenital rectal temperature was 38.5°C, heart rate 180 beats/min diaphragmatic hernia. The foal presented with acute colic and respiratory rate 44 breaths/min. On thoracic and subsequent respiratory distress. There are many causes auscultation, loud tracheobronchial sounds were heard. of colic in the foal and the differential diagnoses depend There was no evidence of wheezes or crackles and the foal did not appear to be in respiratory distress. Mucous membranes were hyperaemic and capillary refill time was *Corresponding author email: [email protected] 3–4 s. The quality of peripheral pulse was good. The

umbilicus and joints were normal on palpation. There was no abdominal distension. Laboratory work on presentation revealed mild dehydration, hypoxaemia, hypercapnia and leucopenia. Packed cell volume was 42% (reference range [rr] 32–46%), total proteins 47 g/l (rr 40–66 g/l), arterial oxygen tension 45.5 mmHg (rr 83–98 mmHg), arterial pCO2 57.1 mmHg (rr 37–43 mmHg) and white blood cell count 2.8 ¥ 109 cells/l (rr 5–12 ¥ 109 cells/l). Blood lactate concentration was mildly elevated; 2.1 mmol/l (rr<2 mmol/l). Serum biochemical analysis was unremarkable. Passive transfer of immunoglobulins was adequate, with serum IgG>8 g/l. A venous blood sample was taken aseptically and submitted for bacterial culture. No growth was reported after 48 h of incubation. The foal’s presenting problems were colic, leucopenia, Fig 1: Latero-lateral projection of the thorax demonstrating hypercapnia and hypoxaemia. The differential diagnoses gas-filled viscera within the thoracic cavity. that were initially considered for the colic included meconium impaction, uroperitoneum, small intestinal volvulus, intussusception, ileus and necrotising enterocolitis The foal’s updated problem list at this point was colic, resulting from hypoxaemia and ischaemia of the bowel. respiratory distress, and progressive hypoxaemia and Leucopenia, hypoxaemia and hypercapnia were initially hypercapnia indicating respiratory failure. The colic was attributed to sepsis and a ventilation perfusion mismatch reassessed by repeating the abdominal ultrasonography, associated with partial lung atelectasis, a focus of performing an abdominocentesis and obtaining pneumonia, or potentially due to pulmonary hypertension radiographs of the abdomen. The respiratory distress with reversion to fetal circulation. and persistent hypoxaemia were investigated further by The initial diagnostic approach to this case was aimed performing thoracic ultrasonographic examination and at determining a cause for the colic as the foal did not thoracic radiography. demonstrate any evidence of respiratory distress at this A repeat abdominal and thoracic ultrasonographic point. examination revealed a distended large colon filled with There was no obvious meconium impaction palpable fluid and distended loops of amotile small intestine. No on digital palpation of the rectum and abdominal free fluid was detected in the abdominal cavity and the palpation was unremarkable. Transabdominal urinary bladder was still intact. Abdominocentesis ultrasonographic examination revealed no abnormalities. revealed no abnormalities. The foal continued to colic The umbilicus appeared ultrasonographically normal and and was treated with 3 mg of butorphanol (Butordol)7 the bladder was intact. There were no amotile loops of i.v. A continuous i.v. infusion of Ringer’s solution was distended small intestine visible or gas lucencies within the initiated at a rate of 4 ml/kg bwt/h. The infusion was wall of the bowel indicating pneumatosis intestinalis. supplemented with 5% glucose at rate of 4 mg/kg bwt/ min to prevent hypoglycaemia. Intranasal oxygen Treatment and outcome insufflation was continued at a rate of 10 l/min. At this point the foal remained weak but made efforts to stand Symptomatic treatment was initiated on admission. A up. central venous catheter (Arrow)1 was placed in the left Thoracic and abdominal radiographs were obtained. jugular vein and intravenous fluid therapy was initiated with On assessment of the radiographs, the presence of boluses of Ringer’s acetate solution2 at a rate of 500 ml q. gas-filled viscera within the thorax was consistent with a 3 h. Intranasal oxygen insufflation was started at a rate diagnosis of a diaphragmatic hernia (Figs 1 and 2). While of 5 l/min. The foal was treated with benzylpenicillin obtaining the ventro-dorsal projections, the foal (Geepenil)3 22,000 iu/kg bwt q.i.d. i.v. and gentamicin deteriorated rapidly and went into respiratory arrest. He (Genta100)4 12 mg/kg bwt s.i.d. i.v. and received a second was intubated immediately and manual intermittent dose of flunixin meglumine (Meflosyl)5 1.1 mg/kg bwt i.v. positive pressure ventilation with 100% oxygen was The phosphate enema (Klyx)6 was also repeated. initiated. After several minutes, the foal’s condition The foal’s condition continued to deteriorate despite stabilised and he was placed on a mechanical ventilator. treatment and 2 h after presentation he began to The ventilator was set on tidal volume of 740 ml (15 ml/kg demonstrate signs of respiratory distress. The mucous bwt) and 15 breaths/min. membranes appeared cyanotic, and the hypoxaemia Immediate surgery was recommended to repair the and hypercapnia became more severe: PaO2 was diaphragmatic hernia but the owner declined and the foal 28.6 mmHg and PaCO2 75.5 mmHg. was subjected to euthanasia.

Fig 2: Latero-lateral projection of the abdomen demonstrating the cranially displaced gas-filled viscera. Fig 4: Photomicrograph of formalin fixed and paraffin embedded tissue of diaphragm at the hernial margin, Masson trichrome staining. The muscle of the diaphragm is stained red (M). A layer of connective tissue, collagen (stained blue) and elastic fibres (unstained), is lining the diaphragmatic muscle on the thoracic side (F). The connective tissue layer is clearly demarcated from the muscle and no inflammation, granulation or scar tissue is present. Bar 500 mm.

Sin Dex No hernial sac was identified, but a round fibrous bundle, 5 mm in width and 15 cm in length, connected the edges of the hernia. The bundle crossed the lumen of the hernia diagonally. The right and quadrate lobes of the liver, 5 m of distal jejunum and the pelvic flexure of the large colon were displaced through the hernial opening and into the thoracic cavity. The herniated organs were congested and the caudal lobes of the lung were atelectatic. No evidence of trauma, scarring or adhesions was present macroscopically in the hernial opening or the herniated organs. Histological examination of the diaphragm at the edge of the hernia revealed a sharply demarcated fibrous lining to the diaphragmatic muscle (Fig 4). On the abdominal side of the diaphragm, the fibrous lining consisted of dense, Dor collagen rich fibrous tissue with a single layer of mesothelial cells superficially. At the margin of the hernial opening, the fibrous layer contained elastic fibres and was continuous Fig 3: Photograph of diaphragm, cranial aspect. An ovoid defect, a with the thoracic side of the diaphragmatic muscle. hernial opening, is located at the sternal part of the diaphragm, on the right side (asterisk). The margins of the defect are smooth and round. A diagonal fibrous bundle is present between the margins of Discussion the hernial opening (arrow). Both congenital and acquired hernias have been reported in horses (Speirs and Reynolds 1976; Collobert et al. 1988; Post mortem findings Proudman and Edwards 1992; Roelvink et al. 1993; Cheetham 1998; Dabareiner and White 1999). Acquired At necropsy, a hernia in the ventral diaphragm was hernias are believed to be caused by a sudden increase in confirmed. The foramen of the hernia was located at the intra-abdominal or intrathoracic pressure. Most acquired sternal part of the diaphragm, to the right of the xiphoid hernias occur in the central part of diaphragm, which is process in the peripheral diaphragm, adjacent to the body thought to be due to the probable weak point at the wall (Fig 3). The foramen of the hernia was 7 ¥ 11 cm in size junction of the muscular and tendinous parts of diaphragm and ovoid in shape, with firm, smooth and rounded edges. (Edwards 1993). In cases of acquired herniation, there is

evidence of trauma or visible laceration of the diaphragm cavity together with parts of the liver. Herniation caused a with histological evidence of inflammation. If chronic, physical obstruction of the intestine and venous occlusion edges of the rent are usually fibrotic and thickened. of the herniated viscera, leading to passive congestion Congenital hernias show no evidence of scarring or and bowel distension. Post mortem examination confirmed adhesions at the margin of the diaphragmatic defect congestion of the herniated viscera. (Brown et al. 2007). In this case, the post mortem The foal in this report developed progressive examination of the diaphragm revealed no evidence of respiratory distress over a period of several hours and trauma or inflammation, confirming that the defect was required supplemental oxygen and ultimately intermittent congenital in origin. positive pressure ventilation to support lung function. Congenital hernias are thought to develop due to the Respiratory distress and reduced exercise tolerance have incomplete fusion of the pleuroperitoneal folds in the fetus. also been reported in other cases of diaphragmatic Therefore, congenital hernias are usually located in the hernia (Speirs and Reynolds 1976; Collobert et al. 1988; dorsal tendinous part of the diaphragm (Speirs and Proudman and Edwards 1992; Edwards 1993; Santschi Reynolds 1976). However, congenital hernias can also et al. 1997; Branson and Kramer 2000). occur due to failure of fusion of the septum transversum Ventilation-perfusion mismatches and mechanical (Speirs and Reynolds 1976; Pauwels et al. 2007) which restriction of lung function resulting in hypoxaemia and usually leads to a diaphragmatic hernia that is located hypercapnia are the most likely reasons for the respiratory ventrally (Collobert et al. 1988; Proudman and Edwards failure in the case. The presence of a diaphragmatic 1992). The hernia in this case was located in the ventral hernia contributes to the respiratory distress in several diaphragm, close to xiphoid cartilage on its right side. This different ways. Viscera in the thoracic cavity interfere suggests that the diaphragmatic hernia in this case with normal chest wall and lung expansion, causing occurred due to the incomplete fusion of the septum decreased lung compliance and essentially creating a transversum. Pauwels et al. (2007) reported 3 cases of form of restrictive pulmonary disease (Rush 2004). congenital retrosternal (Morgagni) diaphragmatic hernia Furthermore, the accompanying alveolar oedema and that were located in the ventral diaphragm in a similar atelectasis causes a reduction in total lung capacity and position to that seen in the foal described in this report. functional residual capacity, leading to significant Interestingly, the retrosternal hernias described by Pauwels ventilation-perfusion mismatches (Rush 2004). Increased et al. (2007) had a hernial sac that was not evident in the intrathoracic pressures and reduced alveolar oxygen foal described in this report. In man, diaphragmatic hernias tension cause an increase in pulmonary vascular located in the ventral part of diaphragm are recognised as resistance (Slack 2009), ultimately leading to pulmonary Morgagni hernias as they protrude through the foramen organ dysfunction and eventual respiratory arrest. Morgagni (Collier 1999). The foramen of Morgagni is a Radiographs were the main diagnostic tool in this case. space located in anterior (ventral) diaphragm between Viscera herniated into thoracic cavity were visible in both xiphoid and costal margins. This space forms when the latero-lateral and ventro-dorsal view. The diaphragmatic muscular part fails to fuse completely during the line was not clear and the thoracic cavity contained development of the diaphragm (París et al. 1973; Collier gas-filled loops of intestines. A normal lung pattern could 1999). In man, over 90% of these hernias are located on the not be seen and instead a mixed alveolar and interstitial right side of the midline (París et al. 1973). Considering pattern was visible due to atelectasis and alveolar the location of the hernia in this foal, the hernia falls into the oedema. Sudden respiratory decompensation occurred category of the Morgagni hernia, but lacked the hernial while the foal was positioned in dorsal recumbency for sac that is almost always present in Morgagni hernias (París radiography of the thorax. Dorsal recumbency has been et al. 1973). A fibrous bundle was identified that crossed reported to decrease arterial oxygen tension in the hernia and could possibly have been the remnants of anaesthetised foals (Braun et al. 2009) and positioning a a ruptured hernial sac. foal with respiratory distress in dorsal recumbency is likely to Diaphragmatic hernias are a rare cause of colic in the exacerbate hypoxaemia by causing compression of the horse and there are only a few reports of diaphragmatic dependent lung fields that will subsequently become hernia causing colic in a neonatal foal (Santschi et al. poorly ventilated resulting in a lower oxygen tension in the 1997; Cheetham 1998). This foal had been born normally pulmonary veins. but appeared weaker than normal from birth and started In retrospect, positioning the foal with respiratory to demonstrate colic signs soon after the birth. The severity distress on dorsal recumbency could have been avoided of the signs is considered to be related to the amount of and would have reduced the likelihood of the foal going viscera herniated and also to the size of the rent (Speirs into respiratory arrest. Latero-lateral projections of the and Reynolds 1976; Edwards 1993). It seems likely that the thoracic cavity were of diagnostic value and a diagnosis viscera in the foal described in this report had already could be made from that projection alone without herniated through the diaphragmatic rent in utero or very subjecting the foal to a period of prolonged dorsal soon after birth. A relatively large proportion of small recumbency. Endotracheal intubation and ventilation with intestine and large colon were herniated into the thoracic 100% oxygen stabilised the foal in this case.

The diagnosis could also potentially have been long-term survival after surgical correction of a achieved using transcutaneous ultrasonography, as diaphragmatic hernia was reported to be low in a recent herniated viscera can, in some cases, be imaged within the case series (Romero and Rodgerson 2010). The prognosis thoracic cavity. A missing diaphragm might be detected for survival of a foal after abdominal surgery depends when the normal diaphragmatic line does not separate largely on the presence of other concurrent diseases in the abdominal and thoracic viscera. The size of the rent could foal. Generally, abdominal surgery in neonatal foals carries also potentially be estimated by counting the intercostal a guarded prognosis (Vatistas et al. 1996; Santschi et al. spaces in which the diaphragm is not visible. 2000). The foal described here was cardiovascularly Ultrasonography also allows better identification of the compromised and general anaesthesia was likely to have herniated viscera compared to radiography and been complicated. The prognosis for the foal would have might provide information about the viability of the also depended largely on the viability of the incarcerated bowel. However, a thorax that appears normal bowel. As in mature horses, the prognosis for survival after ultrasonographically does not exclude a diaphragmatic abdominal surgery in foals is more favourable with hernia, as was the case with this foal. This is probably nonstrangulating lesions of the large bowel compared to because viscera within the thoracic cavity may not be strangulating or primary small intestinal lesions (Vatistas visible if they are not located adjacent to the thoracic wall et al. 1996; Singer and Livesey 1997). (Reef 1998). In this case, the viscera passed through the Congenital diaphragmatic hernia should be diaphragm ventrally and adjacent to the sternum, making considered as a cause of colic in neonatal foals, differentiation between thoracic and abdominal viscera particularly in those individuals that present with difficult. concurrent hypoxaemia, hypercapnia and respiratory Unfortunately surgery was not performed in this case distress. Radiographs were an important diagnostic tool in due to financial constraints and the foal was subjected to this case and should be performed as early as possible in euthanasia at the owner’s request. General anaesthesia order to facilitate a diagnosis. Early surgical intervention of a foal with atelectasis and alveolar oedema is likely to and repair of a congenital diaphragmatic hernia may be complicated due to difficulties inflating the lungs, and carry a favourable prognosis; however, the prognosis is anaesthesia should be maintained with a closed circuit likely to be poor in cases where there are already system and positive pressure ventilation (Scott and ischaemic changes in the herniated viscera. Fishback 1976; Edwards 1993; Branson and Kramer 2000). Authors’ declaration of interests Surgery for diaphragmatic hernias is challenging due to limited access to the defect, especially in mature horses No conflicts of interest have been declared. (Edwards 1993; Malone et al. 2001; Pauwels et al. 2007). Most reports describe an abdominal approach via a ventral midline celiotomy (Scott and Fishback 1976; Speirs Manufacturers’ addresses and Reynolds 1976; Proudman and Edwards 1992; Edwards 1 1993; Santschi et al. 1997; Dabareiner and White 1999). Teleflex medical, Research Triangle Park, North Carolina, USA. 2Baxter International Inc., Deerfield, Illinois, USA. Thoracotomy assisted with thoracoscopy has also been 3Orion Corporation, Espoo, Finland. described in a few reports (Vachon and Fischer 1998; 4CP-Pharma Handelsgesellschaft mbH, Burgdorf, Germany. Malone et al. 2001). In a neonatal foal, the defect is likely 5Fort Dodge Animal Health Holland, Weesp, The Netherlands. to be accessible through a standard abdominal 6Ferring Pharmaceuticals, Saint-Prex, Switzerland. approach. In this foal, the rent was located ventrally and 7Intervet Internation, B.V., Boxmeer, The Netherlands. would probably have been reached without difficulties. The diaphragm can be reconstructed with simple References continuous or interrupted sutures (Speirs and Reynolds 1976; Edwards 1993; Santschi et al. 1997; Freeman 1999). Barton, M.H. (2006) Colic in the newborn foal. In: Equine Neonatal There are also reports that describe repairing the defect by Medicine, Ed: M.R. Paradis, Elsevier, Philadelphia. pp 191-207. using a synthetic mesh that is secured to the margins of the Bernard, W. (2004) Colic in the foal. Equine vet. Educ. 16, 319-323. defect (Scott and Fishback 1976; Dabareiner and White Branson, K.R. and Kramer, J. (2000) Anesthesia case of the month. J. Am. vet. med. Ass. 216, 1918-1919. 1999; Malone et al. 2001). This may be required in cases where the location of the rent makes conventional suturing Braun, C., Trim, C.M. and Egglestone, R.B. (2009) Effects of changing body position on oxygenation and arterial blood pressures in foals impossible or, alternatively, if the surrounding tissues are anesthetized with guaifenesin, ketamine, and xylazine. Vet. fragile and not conducive to closure with sutures. Anaesth. Analg. 36, 18-24. The reported prognosis in cases of a diaphragmatic Brown, C.C., Baker, D.C. and Barker, I.K. (2007) Alimentary system. In: hernia varies in the literature. Prognosis for athletic career Pathology of Domestic Animals, 5th edn., Eds: K.V.F. Jubb, P.C. Kennedy and N. Palmer, Elsevier, Philadelphia. pp 1-296. after successful repair of a diaphragmatic hernia has been Cheetham, J. (1998) Congenital diaphragmatic hernia with subsequent reported to be favourable in some case reports (Santschi incarceration of the left large colon and gastric rupture in a foal. et al. 1997; Dabareiner and White 1999). However, Equine vet. Educ. 10, 239-241.

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Continued from page 332 a MRI examination to identify its extent and location (Ryan References et al. 2011). The cause of the complication in this case was not Hubert, J.D., Burba, D.J. and Moore, R.M. (2006) Evaluation of a vessel determined. There is no reason to believe that a piece of sealing device for laparoscopic granulosa cell tumour removal in standing mares. Vet. Surg. 35, 324-329. intestine or even ovary became lodged within the incision; Lloyd, D., Walmsley, J.P., Greet, T.R.C., Payne, R.J., Newton, J.R. more likely its cause was similar to the process which causes and Phillips, T.J. (2007) Electrosurgery as the sole means of hygroma formation after chronic injury or inflammation. It haemostasis during the laparoscopic removal of pathologically might have been possible to resect the lesion; however, its enlarged ovaries in mare: a report of 55 cases. Equine Vet. J. 39, 210-214. size would have precluded this in a standing patient. Madron, M.S., Caston, S.S., Tracy, A.K. and Kersh, K.D. (2012) Instrument associated complication of a laparoscopic ovariectomy. Equine Vet. Educ. 24, 325-330. Author’s declaration of interests Ryan, E.R., Hosseinzadeh, K., Bansai, M. and Schraut, W.H. (2011) Subperitoneal adenomucinosis following proctocolectomy for No conflicts of interest have been declared. ulcerative colitis. J. Magn. Reson. Imaging 34, 184-188.