abdominal usg foal MCAULIFFE, 2004

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<p>A</p><p>S</p><p>S</p><p>U</p><p>t</p><p>a</p><p>i</p><p>l</p><p>t</p><p>fi</p><p>t</p><p>fi</p><p>T</p><p>o</p><p>n</p><p>c</p><p>t</p><p>b</p><p>l</p><p>v</p><p>U</p><p>i</p><p>g</p><p>l</p><p>i</p><p>T</p><p>A</p><p>3</p><p>bdominal Ultrasonography of the Foal</p><p>iobhan B. McAuliffe, MVB</p><p>Disorders of abdominal organs represent a large proportion of diseases encountered in</p><p>equine neonatal medicine. Ultrasonography was first used in the equine neonate for the</p><p>diagnosis of internal umbilical remnant infections and has since been used for the diag-</p><p>nosis of a wide variety of disorders. Ultrasound is noninvasive, well tolerated by the foal,</p><p>and easily performed in the field. In addition, the smaller size of the foal abdomen and</p><p>proximity of many organs of interest makes the foal an ideal candidate for abdominal</p><p>ultrasonography. These factors have led to increasing use of ultrasonography in the equine</p><p>neonate; with this increased use has come awareness of the prognostic as well as</p><p>diagnostic features of ultrasound. This article reviews the technique for abdominal ultra-</p><p>sonography, including its advantages and limitations, and provides an overview of neces-</p><p>sary equipment. The ultrasonographic appearance of abdominal organs under normal and</p><p>pathologic conditions is also described.</p><p>Clin Tech Equine Pract 3:308-316 © 2004 Elsevier Inc. All rights reserved.</p><p>KEYWORDS ultrasonography, neonate, abdominal, renal, umbilical, hepatic</p><p>U</p><p>T</p><p>e</p><p>m</p><p>t</p><p>v</p><p>i</p><p>e</p><p>o</p><p>m</p><p>u</p><p>o</p><p>i</p><p>s</p><p>d</p><p>d</p><p>g</p><p>n</p><p>c</p><p>i</p><p>t</p><p>b</p><p>u</p><p>s</p><p>t</p><p>i</p><p>t</p><p>m</p><p>i</p><p>canning Technique</p><p>ltrasonographic examination of the abdominal organs</p><p>has been well described in foals.1-6 Sector and linear</p><p>ransducers can be used, and both produce high-quality im-</p><p>ges. Sector scanners have a small footprint that facilitates</p><p>ntercostal imaging. Linear transducers produce a rectangu-</p><p>ar image that is well suited for examining superficial struc-</p><p>ures; however, with increasing depth, the image of the far</p><p>eld is narrowed which restricts visualization of deep struc-</p><p>ures. Curved linear transducers provide wide near and far</p><p>elds of view, and the footprint size is usually intermediate.</p><p>he highest frequency transducer that penetrates to the area</p><p>f interest should be used and the smallest depth of field</p><p>ecessary should be displayed.</p><p>Sedation is not generally required but may be necessary in</p><p>ertain individuals. For optimal image quality, the entire ven-</p><p>ral abdomen should be clipped with a #40 surgical clipper</p><p>lade from the xiphoid caudally to the inguinal region. The</p><p>ateral abdomen and paralumbar fossa should also be clipped</p><p>entral to a line drawn from the tuber coxae to the elbow.</p><p>ltrasound coupling gel should be applied following wash-</p><p>ng of the abdomen with warm water. Examination of the</p><p>astrointestinal viscera is performed from the most ventral</p><p>ocation to avoid interference from gas present in the gastro-</p><p>ntestinal viscera that rises dorsally.</p><p>he Stables of HRH Crown Prince Abdullah bin Abdul Aziz & Sons, Riyadh.</p><p>ddress reprint requests and correspondence to: Siobhan B. McAuliffe,</p><p>MVB, The Stables of HRH Crown Prince Abdullah bin Abdul Aziz &</p><p>Sons, PO Box 46935, Riyadh, Kingdom of Saudi Arabia, 11542. E-mail:</p><p>wsiobhanmcauliffe@hotmail.com</p><p>08 1534-7516/04/$-see front matter © 2004 Elsevier Inc. All rights reserved.</p><p>doi:10.1053/j.ctep.2005.02.008</p><p>mbilical Remnants</p><p>he umbilical vein is located along the midline from the</p><p>xternal umbilicus to the liver and becomes the round liga-</p><p>ent of the liver. It is a small oval or elliptical vessel with a</p><p>hin echogenic wall and an anechoic center. The umbilical</p><p>ein usually measures 10 mm or less in diameter throughout</p><p>ts length.7 The umbilical arteries course caudally from the</p><p>xternal umbilical remnant and become the round ligaments</p><p>f the bladder. They are thick walled with a diameter of 12</p><p>m or less and commonly contain an echogenic clot. The</p><p>rachus retracts after birth and becomes the median ligament</p><p>f the bladder. In the normal foal, it contains no fluid.</p><p>Umbilical remnant infections may be external (Fig. 1),</p><p>nternal, or both and have frequently been incriminated as a</p><p>ource of septicemic infections.8 External infections may be</p><p>etected clinically in the presence of heat, pain, swelling, or</p><p>ischarging purulent material or can be diagnosed ultrasono-</p><p>raphically as an enlarged thickened external umbilical rem-</p><p>ant containing hypoechoic to echogenic fluid.8 Hypere-</p><p>hoic echoes representing gas may be detected and are</p><p>ndicative of an anaerobic infection if there is no gas-filled</p><p>ract extending from the skin surface into the external um-</p><p>ilical remnant.9 Internal infections are best diagnosed with</p><p>ltrasonography. Enlargement of any of the internal remnant</p><p>tructures, with the detection of intraluminal fluid, indicates</p><p>he presence of infection. Involvement of multiple structures</p><p>s common in foals with internal umbilical remnant infec-</p><p>ion.1,2,8 Infection of the urachus and umbilical arteries is</p><p>ost common, with less frequent involvement of the umbil-</p><p>cal vein.8 The infected umbilical vein is enlarged (�10 mm)</p><p>ith the most prominent enlargement at or near the external</p><p>u</p><p>c</p><p>u</p><p>s</p><p>s</p><p>e</p><p>l</p><p>c</p><p>e</p><p>i</p><p>e</p><p>i</p><p>e</p><p>f</p><p>b</p><p>s</p><p>e</p><p>t</p><p>f</p><p>U</p><p>H</p><p>s</p><p>l</p><p>i</p><p>fl</p><p>v</p><p>w</p><p>s</p><p>P</p><p>D</p><p>A</p><p>b</p><p>u</p><p>c</p><p>c</p><p>U</p><p>T</p><p>8</p><p>b</p><p>d</p><p>a</p><p>d</p><p>a</p><p>a</p><p>c</p><p>h</p><p>e</p><p>o</p><p>F</p><p>b</p><p>F</p><p>f</p><p>w</p><p>u</p><p>c</p><p>a</p><p>h</p><p>t</p><p>e</p><p>a</p><p>p</p><p>F</p><p>N</p><p>t</p><p>Abdominal ultrasonography of the foal 309</p><p>mbilical remnant. The luminal contents can vary from ane-</p><p>hoic to echogenic material. Thickening of the walls of the</p><p>mbilical vein is likely with longstanding infection. Exten-</p><p>ion cranially into the liver may result in hepatic abscesses or</p><p>uppurative hepatitis and warrants a thorough sonographic</p><p>xamination of the liver. An infected umbilical artery is en-</p><p>arged (�13 mm) with a thickened wall and contains ane-</p><p>hoic to echoic fluid. Although the greatest increase in diam-</p><p>ter of the artery may occur anywhere along its length, the</p><p>nfected umbilical artery is usually largest just caudal to the</p><p>xternal umbilical remnant or at the apex of the bladder.1 An</p><p>nfected urachus is enlarged and filled with anechoic, hypo-</p><p>choic, or echogenic fluid (Fig. 2). A combined measurement</p><p>or the urachus and both umbilical arteries at the apex of the</p><p>igure 1 Enlarged external umbilicus in a foal with an external um-</p><p>ilical remnant infection.</p><p>igure 2 Sonogram of the urachus and both umbilical arteries in a</p><p>oal with urachitis and omphaloarteritis. Notice the enlarged thick</p><p>alled urachus (large arrows) filled with hypoechoic fluid. The</p><p>mbilical arteries are the small echoic structures with the hypere-</p><p>hoic rim along the endothelium of the vessel. The left umbilical</p><p>rtery (the small arrow to the right) is enlarged and filled with</p><p>ypoechoic fluid, while the right umbilical artery (the small arrow</p><p>o the left) is normal size but also contains a small amount of hypo-</p><p>choic fluid. This is a transverse sonogram with the right side of the</p><p>bdomen displayed on the left side of the sonogram. (Image sup-</p><p>dlied courtesy of Dr. Virginia B. Reef.)</p><p>ladder greater than 25 mm indicates infection.1,8 Long-</p><p>tanding infections may become walled off and appear as</p><p>ncapsulated abscesses. Identification of infection of any of</p><p>he internal umbilical remnants should be followed by care-</p><p>ul examination of adjacent organs.</p><p>mbilical Remnant Hemorrhage</p><p>emorrhage from the umbilical cord at parturition may re-</p><p>ult in swelling of the internal umbilical vessels or perivascu-</p><p>ar tissues. Rupture of the umbilical vein or artery may result</p><p>n hemoabdomen which is imaged as echogenic swirling</p><p>uid (Fig. 3) within the peritoneal cavity, or a large area of</p><p>ascular and perivascular hemorrhage may be imaged with or</p><p>ithout a fibrin clot.1,2 Occasionally, fibrin clots may be vi-</p><p>ualized in the bladder or urachus.</p><p>atent Urachus and Urachal</p><p>iverticulum</p><p>nechoic fluid within the urachus that is continuous with the</p><p>ladder apex and external umbilicus is indicative of a patent</p><p>rachus. A urachal diverticulum is a fluid-filled caudal ura-</p><p>hus continuous with the bladder apex and has been impli-</p><p>ated as a cause of stranguria in the foal.2</p><p>rinary Bladder</p><p>he bladder is adjacent to the ventral abdominal wall for 4 to</p><p>weeks after birth; thereafter, the large colon is interspersed</p><p>etween the bladder and ventral abdominal wall. The blad-</p><p>er can still be visualized</p><p>in the caudoventral and midlateral</p><p>bdomen in foals up to 6 months of age. Maximal bladder</p><p>istension in 1- and 7-day-old foals has been reported as 9</p><p>nd 10 cm, respectively.5</p><p>Ultrasound has become extremely useful in detecting uro-</p><p>bdomen associated with defects of the bladder wall or ura-</p><p>hus. Uroperitoneum has been recognized in otherwise</p><p>ealthy and hospitalized neonates. Affected foals that are oth-</p><p>rwise healthy are most commonly male, less than 1 week</p><p>ld, with a history of stranguria and progressive abdominal</p><p>igure 3 Sonogram of the abdomen from a foal with hemoabdomen.</p><p>otice the large amount of echoic fluid surrounding the collapsed</p><p>hickened loops of small intestine (small arrows).</p><p>istention. These foals typically develop hyponatremia, hy-</p><p>p</p><p>t</p><p>g</p><p>r</p><p>p</p><p>h</p><p>d</p><p>w</p><p>l</p><p>r</p><p>a</p><p>u</p><p>s</p><p>t</p><p>e</p><p>d</p><p>i</p><p>u</p><p>4</p><p>t</p><p>r</p><p>fl</p><p>g</p><p>fl</p><p>fl</p><p>d</p><p>l</p><p>d</p><p>n</p><p>s</p><p>s</p><p>fl</p><p>r</p><p>w</p><p>u</p><p>u</p><p>t</p><p>p</p><p>i</p><p>d</p><p>w</p><p>t</p><p>K</p><p>T</p><p>p</p><p>f</p><p>r</p><p>h</p><p>I</p><p>2</p><p>c</p><p>6</p><p>a</p><p>r</p><p>a</p><p>r</p><p>m</p><p>c</p><p>h</p><p>h</p><p>t</p><p>s</p><p>r</p><p>t</p><p>f</p><p>u</p><p>o</p><p>b</p><p>t</p><p>d</p><p>s</p><p>n</p><p>F</p><p>N</p><p>a</p><p>s</p><p>F</p><p>t</p><p>f</p><p>i</p><p>c</p><p>fl</p><p>310 S.B. McAuliffe</p><p>ochloremia, hyperkalemia, and azotemia. Hospitalized pa-</p><p>ients that developed uroperitoneum showed no significant</p><p>ender predilection in one study, and there was a significant</p><p>elationship between sepsis and uroperitoneum.10 In these</p><p>atients, the development of the disorder is postulated to</p><p>ave two etiologies: one is ischemia and necrosis of the blad-</p><p>er wall and the other is manipulation of obtunded patients</p><p>ith distended bladders. The clinical chemistry findings are</p><p>ess consistent in this group and may be related to earlier</p><p>ecognition in hospitalized patients or concurrent fluid ther-</p><p>py for other disorders.</p><p>In addition to the noninvasive nature of the procedure,</p><p>ltrasonography is useful in locating the site of the defect for</p><p>urgical repair, with a significant relationship existing be-</p><p>ween the ultrasound findings and lesion location at surgical</p><p>xploration.10 The most common defect is in the dorsal blad-</p><p>er wall. Defects of the ureters are less common, and congen-</p><p>tal causes of uroabdomen have also been reported.11 The</p><p>ltrasound image obtained shows free peritoneal fluid (Fig.</p><p>). The volume and character of the fluid vary depending on</p><p>he time course involved: small amounts of anechoic fluid in</p><p>ecent onset uroabdomen to large amounts of hypoechoic</p><p>uid with fibrin strands if secondary peritonitis exists. The</p><p>astrointestinal viscera are seen floating in the abdominal</p><p>uid (Fig. 4), and the urinary bladder can also be imaged</p><p>oating in the fluid. Depending on the size and location of the</p><p>efect, the bladder may contain anechoic urine or be col-</p><p>apsed and folded on itself (Fig. 5). This folding of the blad-</p><p>er wall is characteristic of a bladder wall defect and should</p><p>ot be confused with a recently voided bladder, which has a</p><p>mall contracted appearance but does not appear folded.</p><p>Defects in the urachus result in dissection of fluid into the</p><p>urrounding tissues, and the bladder usually has a round and</p><p>uid-filled appearance, as the defects are generally small and</p><p>esult in slow leakage of urine into the peritoneal cavity. Foals</p><p>hich have a normal appearance of both the bladder and</p><p>rachal remnants with uroperitoneum are likely to have a</p><p>reteral defect.6 The ureters are not normally visible, and</p><p>hus direct imaging of the defect with ultrasonography is not</p><p>igure 4 Sonogram of the abdomen from a foal with uroperitoneum.</p><p>otice the large amount of anechoic fluid in the abdominal cavity</p><p>nd the loops of jejunum (arrows) floating within the fluid. (Image</p><p>upplied courtesy of Dr. Virginia B. Reef.)</p><p>ossible. Attempts to identify the location of the defect are t</p><p>mportant as nonsurgical treatment of urachal and ureteral</p><p>efects may be successful. Medical treatment of a bladder</p><p>all defect in a critically ill foal has also been reported, but</p><p>hese defects generally require surgical intervention.12</p><p>idneys</p><p>he right kidney is located ventral to the transverse spinous</p><p>rocesses between the 14th and 16th intercostal spaces (ICS)</p><p>rom 2 cm dorsal to the tuber coxae to 12 cm ventral. The</p><p>ight kidney has a heart-shaped appearance. The left kidney</p><p>as a bean-shaped appearance and is located from the 15th</p><p>CS to the caudal border of the left paralumbar fossa and from</p><p>cm dorsal to 15 cm ventral to the dorsal margin of the tuber</p><p>oxae. Measurement of kidney length and width in foals up to</p><p>months of age showed a significant difference between right</p><p>nd left kidneys, with the left kidney being longer and the</p><p>ight kidney being wider for all age groups.5 The renal pelvis</p><p>nd calices are hyperechoic, the renal cortex is hypoechoic in</p><p>elation to the renal calices, and the renal medullary pyra-</p><p>ids are relatively anechoic, allowing for a prominent corti-</p><p>omedullary junction. The renal capsule is imaged as a thin</p><p>yperechoic line surrounding the kidney. As in mature</p><p>orses, the echogenicity of the renal cortex is less than that of</p><p>he liver, which in turn is less than that of the spleen.13</p><p>Congenital renal defects that may be detected by ultra-</p><p>ound include renal cysts, renal hypoplasia, renal dysplasia,</p><p>enal agenesis, renal arteriovenous malformation, and ec-</p><p>opic ureters. Measurements of renal length and width for</p><p>oals up to 6 months of age have been reported, with contin-</p><p>al growth of both kidneys in that time frame.5 Renal hyp-</p><p>plasia is recognized as a smaller than normal kidney and can</p><p>e unilateral or bilateral.14 Renal dysplasia is recognized ul-</p><p>rasonographically as misshapen, hyperechoic kidneys with</p><p>ecreased corticomedullary demarcation.15,16 Renal agenesis</p><p>hould be considered when a kidney cannot be found in a</p><p>ormal or ectopic location. In humans and small animals, the</p><p>igure 5 Sonogram of the bladder obtained transcutaneously from</p><p>he ventral abdomen of a foal with a ruptured bladder. Notice the</p><p>olded appearance of the ruptured bladder floating in the surround-</p><p>ng anechoic fluid. The defect in the dorsal wall of the bladder is not</p><p>learly visible but is adjacent to the tip of the arrow. In real-time,</p><p>uid was imaged passing through this defect. (Image supplied cour-</p><p>esy of Dr. Virginia B. Reef.)</p><p>c</p><p>v</p><p>H</p><p>a</p><p>t</p><p>n</p><p>b</p><p>c</p><p>H</p><p>h</p><p>t</p><p>r</p><p>f</p><p>s</p><p>a</p><p>f</p><p>r</p><p>o</p><p>a</p><p>t</p><p>t</p><p>o</p><p>c</p><p>f</p><p>f</p><p>r</p><p>m</p><p>g</p><p>n</p><p>L</p><p>T</p><p>a</p><p>1</p><p>c</p><p>l</p><p>c</p><p>w</p><p>v</p><p>c</p><p>p</p><p>T</p><p>h</p><p>t</p><p>a</p><p>d</p><p>o</p><p>m</p><p>f</p><p>t</p><p>p</p><p>m</p><p>h</p><p>b</p><p>b</p><p>m</p><p>o</p><p>t</p><p>o</p><p>s</p><p>a</p><p>p</p><p>m</p><p>h</p><p>s</p><p>a</p><p>c</p><p>g</p><p>v</p><p>T</p><p>d</p><p>c</p><p>p</p><p>b</p><p>e</p><p>e</p><p>a</p><p>o</p><p>r</p><p>c</p><p>d</p><p>a</p><p>o</p><p>r</p><p>T</p><p>w</p><p>S</p><p>T</p><p>b</p><p>t</p><p>i</p><p>t</p><p>i</p><p>e</p><p>r</p><p>h</p><p>G</p><p>T</p><p>s</p><p>d</p><p>d</p><p>r</p><p>s</p><p>g</p><p>t</p><p>n</p><p>Abdominal ultrasonography of the foal 311</p><p>ontralateral kidney hypertrophies with time. Renal arterio-</p><p>enous malformation has been recognized in a Quarter</p><p>orse. Color flow Doppler ultrasonography demonstrated an</p><p>nomalous vascular connection between artery and vein of</p><p>he affected kidney.17 Direct imaging of ectopic ureters is not</p><p>ormally possible but ultrasound guided pyelography has</p><p>een used to diagnose ectopic ureters.18</p><p>Renal disease is relatively common in neonatal foals asso-</p><p>iated with peripartum asphyxia and hypoxic renal injury.</p><p>owever, ultrasound evaluation of the kidneys in these foals</p><p>as not demonstrated consistent findings. Enlarged kidneys</p><p>hat are less echogenic than normal and consistent with acute</p><p>enal failure have been seen in some foals; while in other</p><p>oals, there have been no abnormalities detected or only a</p><p>light increase in parenchymal echogenicity.1,4,19 Recently,</p><p>ssessment of renal blood flow as an indication of acute renal</p><p>ailure in foals has become more commonplace in large refer-</p><p>al institutions, but to date there has been no controlled study</p><p>f its prognostic value. Children with acute renal failure have</p><p>n absence of blood flow in late diastole or throughout dias-</p><p>ole that is easily detected with Doppler ultrasound.20,21</p><p>Renal failure secondary to the administration of nephro-</p><p>oxic drugs is also of great importance in foals. Development</p><p>f a diffuse hyperechoic zone in the renal medulla near the</p><p>orticomedullary junction has been reported in two of three</p><p>oals administered phenylbutazone at 5 mg/kg body weight</p><p>or 7 days. These foals did not demonstrate clinical signs of</p><p>enal failure, and the ultrasound changes were correlated to</p><p>ineralization in the collecting tubules of the medullary re-</p><p>ion. The potential clinical significance of these changes was</p><p>ot determined.22</p><p>iver</p><p>he liver can normally be seen in the cranioventral and mid-</p><p>bdomen between the 7th and 14th ICS and dorsally in the</p><p>4th ICS on the right side of the abdomen. On the left side, it</p><p>an be seen between the 6th and 10th ventrolateral ICS in a</p><p>arger area compared with mature animals.5 Hepatic vessels</p><p>an be seen diffusely throughout the liver parenchyma. The</p><p>alls of the portal veins are more echogenic than the hepatic</p><p>eins as they are surrounded by more connective tissue.23</p><p>Portosystemic shunts are anomalies of the portosystemic</p><p>irculation that allow direct communication between the</p><p>ortal circulation and a systemic vein such as the vena cava.</p><p>hese anomalies are rare in horses, and diagnosis is based on</p><p>istory, clinical signs, clinical pathology, and contrast por-</p><p>ography.24,25 Doppler ultrasonography may be a useful di-</p><p>gnostic aid and has commonly been used in dogs for the</p><p>etection of extrahepatic shunts.26 Intrahepatic shunts and</p><p>ther vascular anomalies are more difficult to detect.</p><p>Tyzzer’s disease in foals is an acute bacterial hepatitis,</p><p>yocarditis, and /or colitis and has been reported in foals</p><p>rom 7 to 92 days of age. Ante-mortem diagnosis is difficult as</p><p>here is no rapid definitive diagnostic test. It should be sus-</p><p>ected in any foal with acute hepatic failure, hepatic enlarge-</p><p>ent, and a diffuse increase in parenchymal echogenicity.27</p><p>Septicemia in foals may result in bacterial hepatitis via</p><p>ematogenous inoculation. Many species of bacteria have</p><p>een incriminated, but Actinobacillus equuli in particular has</p><p>een associated with hepatitis and nephritis, characterized by u</p><p>ultifocal abscessation with an ultrasonographic appearance</p><p>f multiple small areas of increased echogenicity scattered</p><p>hroughout the hepatic parenchyma.1</p><p>Hepatic abscesses, although rare in foals, can occur sec-</p><p>ndary to ascending umbilical vein infections or as a progres-</p><p>ion of a suppurative hepatitis.8 When detected early, these</p><p>bscesses are hypoechoic with ill defined margins; as they</p><p>rogress and become surrounded by more echogenic inflam-</p><p>atory tissue, they become better defined.1</p><p>Portal vein thrombosis has been reported in calves with</p><p>epatic abscessation and in one foal with an umbilical ab-</p><p>cess, Streptococcus zooepidemicus cellulitis and pneumonia,</p><p>nd Rhodococcus equi polyarthritis and pneumonia.24 In this</p><p>ase, the hepatic parenchyma appeared normal ultrasono-</p><p>raphically with a thrombus occupying 90% of the portal</p><p>ein, as well as the primary intrahepatic portal vein branches.</p><p>reatment consisted of antibiotics and antiinflammatory</p><p>rugs. Repeat ultrasound examinations demonstrated a re-</p><p>annulization of the portal vein and the development of hy-</p><p>erechogenic foci in the liver parenchyma. With the throm-</p><p>us resolved, the liver enzymes, which had initially been</p><p>levated, declined, and despite the presence of abnormal</p><p>chogenic foci in the liver, no permanent hepatic function</p><p>bnormalities were detected.24</p><p>Cholangiohepatitis has been reported in foals as a sequela</p><p>f gastroduodenal ulceration.24 Duodenal strictures occur-</p><p>ing secondary to gastroduodenal ulceration can lead to</p><p>holangiohepatitis through two mechanisms. If the stricture</p><p>evelops at the hepaticoduodenal area, bile duct obstruction</p><p>nd ascending cholangiohepatitis can follow. Strictures that</p><p>ccur aborad to the bile duct can result in bile stasis and</p><p>eflux of ingesta into the bile duct with ascending infection.</p><p>hickening of the bile ducts with echogenic material imaged</p><p>ithin the biliary tree is indicative of cholangiohepatitis.1,6</p><p>pleen</p><p>he spleen is imaged between the 7th ICS and the paralum-</p><p>ar fossa (PLF) on the left side and in the 9th ventral ICS on</p><p>he right side in contact with the liver. The splenic vein is</p><p>maged on the medial aspect of the spleen, caudal and dorsal</p><p>o the stomach in the 11th to 12th mid-ICS. The spleen</p><p>nterfaces caudally with the left kidney and is homogenously</p><p>chogenic, with few vessels seen.5 Splenic abnormalities are</p><p>are in foals. Trauma resulting in a splenic hematoma and/or</p><p>emoabdomen may occur.</p><p>astrointestinal Viscera</p><p>he clinical signs of abdominal visceral disease may be mild,</p><p>uch as decreased nursing or lethargy, and can be difficult to</p><p>istinguish from signs associated with other neonatal disor-</p><p>ers. Abdominal disorders are common in the neonatal pe-</p><p>iod, and thorough evaluation of the gastrointestinal tract</p><p>hould be performed in all foals with signs referable to the</p><p>astrointestinal tract or in those with nonspecific signs. Due</p><p>o their small size and proximity of many organs of interest,</p><p>eonatal foals are ideal candidates for ultrasonographic eval-</p><p>ation of the viscera.</p><p>S</p><p>T</p><p>v</p><p>s</p><p>v</p><p>h</p><p>t</p><p>p</p><p>a</p><p>w</p><p>t</p><p>a</p><p>i</p><p>s</p><p>i</p><p>c</p><p>r</p><p>t</p><p>o</p><p>T</p><p>t</p><p>o</p><p>m</p><p>U</p><p>d</p><p>a</p><p>i</p><p>s</p><p>c</p><p>d</p><p>t</p><p>i</p><p>a</p><p>v</p><p>S</p><p>S</p><p>f</p><p>M</p><p>l</p><p>S</p><p>I</p><p>b</p><p>s</p><p>r</p><p>s</p><p>r</p><p>i</p><p>p</p><p>d</p><p>l</p><p>a</p><p>U</p><p>U</p><p>d</p><p>a</p><p>h</p><p>d</p><p>t</p><p>h</p><p>c</p><p>a</p><p>t</p><p>v</p><p>f</p><p>d</p><p>u</p><p>u</p><p>N</p><p>o</p><p>o</p><p>s</p><p>w</p><p>f</p><p>s</p><p>o</p><p>g</p><p>S</p><p>e</p><p>(</p><p>b</p><p>a</p><p>t</p><p>i</p><p>I</p><p>T</p><p>w</p><p>b</p><p>c</p><p>F</p><p>n</p><p>s</p><p>e</p><p>p</p><p>312 S.B. McAuliffe</p><p>tomach</p><p>he stomach is located medial to the spleen in the mid- to</p><p>entral abdomen between the 6th and 12th ICS on the left</p><p>ide. The ventral wall of the stomach is in contact with the</p><p>entral abdomen up to 7 days of age.5 The stomach wall is</p><p>ypoechoic relative to surrounding structures. In foals less</p><p>han 7 days, luminal contents are visible. In older foals, the</p><p>resence of gas prevents imaging of the gastric contents, and</p><p>t this stage, the foal’s stomach resembles that of an adult</p><p>ith a large curvilinear echo medial to the spleen and caudal</p><p>o the liver. Ultrasonographic examination of the stomach is</p><p>n essential part of sonographic examination of the abdomen</p><p>n foals with suspected abdominal disease. Distention of the</p><p>tomach may be pronounced and easily detected with small</p><p>ntestinal obstructions. Gastric and duodenal distention is</p><p>ommonly seen in foals with gastroduodenal ulcers. Gastric</p><p>upture may occur secondary to gastric ulceration or obstruc-</p><p>ive disorders. A marked increase in peritoneal fluid is noted</p><p>n sonographic examination in foals with a ruptured viscus.</p><p>he character of the fluid is highly variable and depends on</p><p>he age of the foal (predominantly milk diet) and the duration</p><p>f the rupture. Exsanguination with a resultant hemoabdo-</p><p>en secondary to gastric ulceration has also been reported.28</p><p>ltrasonography has also been used in dogs and humans to</p><p>etect gastric ulceration, with or without perforation.29,30</p><p>The small intestine can be visualized in a larger area of the</p><p>bdomen in young foals compared with adults. The small</p><p>ntestine has a hypoechoic wall and its lumen is easily ob-</p><p>erved. The duodenum is visualized between the ventral and</p><p>audal aspect of the liver and the dorsal margin of the right</p><p>orsal colon. It can also be seen ventral to the caudal pole of</p><p>he right kidney and dorsal to the cecal base.5 The large</p><p>ntestine is recognized by its larger diameter and sacculated</p><p>ppearance. The lumen of the large intestine is not normally</p><p>isualized due to the presence of gas.</p><p>mall Intestinal Disorders</p><p>mall intestinal disorders are common in foals and range</p><p>rom congenital defects, such as scrotal/inguinal hernias and</p><p>eckel’s diverticulum, to enteritis, ascarid impaction, volvu-</p><p>us, intussusception, or abdominal abscesses.31-33</p><p>crotal/Inguinal Hernias</p><p>nguinal hernias are generally noticed within a few days of</p><p>irth as soft fluctuant swellings in the inguinal region and</p><p>crotum. The hernia can be easily reduced when the foal is</p><p>olled onto its back. Scrotal hernias in foals usually resolve</p><p>pontaneously and incarceration of intestine in the hernia is</p><p>are. Ultrasonography can be used to characterize the viabil-</p><p>ty of incarcerated bowel in these rare instances; with com-</p><p>romised bowel having a thickened and edematous wall and</p><p>ecreased to absent peristaltic movement. Color flow Dopp-</p><p>er can also be used to assess the blood flow of the incarcer-</p><p>ted segment.34</p><p>mbilical Hernia</p><p>mbilical hernias are the second most common congenital</p><p>efect in horses (cryptorchidism is the most common) with a</p><p>n incidence of 0.5% to 2%.30 The majority of umbilical</p><p>ernias are small (�2.5 cm in diameter) and are easily re-</p><p>uced. Ultrasonography is used in addition to digital palpa-</p><p>ion to determine the size of the defect. The contents of the</p><p>ernial sac (fluid, omentum, or intestine) and the presence of</p><p>oncurrent internal umbilical or subcutaneous infection can</p><p>lso be assessed ultrasonographically. Determining the size of</p><p>he defect by measuring the diameter in a sagittal and trans-</p><p>erse plane aids in selecting the most appropriate procedure</p><p>or closure. The uncomplicated umbilical hernia appears as a</p><p>efect in the ventral abdominal wall, whereas a complicated</p><p>mbilical hernia also has infection of the internal or external</p><p>mbilical remnants or adjacent subcutaneous structures.</p><p>onreducible umbilical hernias can occur with strangulation</p><p>r incarceration of omentum, small intestine, ventral colon,</p><p>r cecum within the hernial sac. Strangulation should be</p><p>uspected in a nonreducible hernia that increases in size,</p><p>armth, and becomes painful, hot, and edematous. Such</p><p>oals often present with or have a history of colic, but the</p><p>everity of pain is not a reliable indicator of strangulation or</p><p>ther complications.35 Fat contained within the omentum</p><p>ives a heterogeneous hypoechoic to echogenic appearance.</p><p>trangulated ileum (most common) or jejunum has a thick-</p><p>ned, edematous wall with decreased or absent motility</p><p>Figs. 6 and 7).1 Color flow Doppler can also be used to assess</p><p>owel viability in such cases.34 If large bowel is involved, only</p><p>portion of the ventral colon or cecum is incarcerated within</p><p>he hernia and is imaged as an outpouching of the large</p><p>ntestine with thickened, edematous, and amotile walls.</p><p>ntussusception</p><p>he use of ultrasound to detect intussusceptions in foals is</p><p>ell reported with a characteristic “bull’s eye” or “target” sign</p><p>eing obtained by scanning through the apex of the intussus-</p><p>eption where the intussusceptum is surrounded by fluid</p><p>igure 6 Sonogram of the abdomen obtained from a foal with a</p><p>onreducible umbilical hernia. There is an incarcerated loop of</p><p>mall intestine present within the umbilical hernia. Notice the thick-</p><p>ned edematous wall of the small intestine and the surrounding</p><p>eritoneal fluid within the hernial sac.</p><p>nd the intussuscipiens (Figs. 8 and 9).1,2,36 Different sono-</p><p>g</p><p>t</p><p>t</p><p>b</p><p>o</p><p>c</p><p>S</p><p>V</p><p>F</p><p>w</p><p>d</p><p>a</p><p>v</p><p>v</p><p>m</p><p>P</p><p>d</p><p>r</p><p>t</p><p>o</p><p>I</p><p>S</p><p>v</p><p>p</p><p>a</p><p>a</p><p>b</p><p>t</p><p>m</p><p>t</p><p>t</p><p>o</p><p>E</p><p>T</p><p>fi</p><p>t</p><p>e</p><p>F</p><p>f</p><p>a</p><p>F</p><p>i</p><p>a</p><p>p</p><p>F</p><p>f</p><p>F</p><p>l</p><p>t</p><p>a</p><p>Abdominal ultrasonography of the foal 313</p><p>raphic appearances may be obtained depending on the por-</p><p>ion of the intussusception being imaged. Jejunojejunal in-</p><p>ussusceptions are most common in young foals and have</p><p>een linked to bacterial and protozoal infections, and the use</p><p>f prokinetic drugs. Ileo-ileal and ileo-cecal intussusceptions</p><p>an also be seen in older foals, weanlings, and yearlings.</p><p>mall Intestinal</p><p>olvulus/Obstruction</p><p>luid-filled, amotile small intestine with thicker than normal</p><p>alls is suggestive of a small intestine volvulus (Fig. 10). The</p><p>egree of wall thickness increases with the passage of the time</p><p>nd the wall may be of normal thickness soon after the vol-</p><p>ulus occurs making differentiation from ileus difficult. Vol-</p><p>ulus is most often seen in foals less than 3 months of age and</p><p>ay affect the entire small intestine or only a small portion.</p><p>ain is severe and the clinical condition of these foals rapidly</p><p>eteriorates. Meckel’s diverticulum and other embryologic</p><p>emnants may cause small intestine obstruction resulting in</p><p>igure 7 Intraoperative picture of the incarcerated small intestine</p><p>rom the foal in Figure 6. Note the thickened edematous bowel wall</p><p>nd congestion of the associated blood vessels.</p><p>igure 8 Sonogram of the abdomen obtained from a foal with a small</p><p>ntestinal intussusception. Notice the “target” or “bull’s eye” appear-</p><p>nce of the small intestinal intussusception (arrow). Three different</p><p>ortions of the intussusception are depicted in sonographic image. t</p><p>hickened, amotile intestine proximal to and in the area of the</p><p>bstruction.</p><p>leus</p><p>onographic examination of foals with ileus usually re-</p><p>eals bowel with an increased diameter and little if any</p><p>eristaltic activity.1,2 The intestinal wall thickness is usu-</p><p>lly normal but may be increased with certain etiologies,</p><p>nd other intestinal or peritoneal fluid abnormalities may</p><p>e detected. Mechanical ileus associated with intussuscep-</p><p>ions, volvulus, obstructive embryonic remnants, mural</p><p>asses, meconium or ascarid impactions, and trichophy-</p><p>obezoars produces segmental dilation; whereas func-</p><p>ional ileus associated with hypoxic bowel injury, surgery,</p><p>r anesthesia produces generalized distention.</p><p>nteritis</p><p>he sonographic appearance of enteritis is variable, but fluid-</p><p>lled hypermotile bowel is usually present. Intestinal wall</p><p>hickness is also variable but is generally symmetric. Many</p><p>tiologies have been implicated in the development of enter-</p><p>igure 9 Intraoperative picture of an ileo-ileal intussusception in a</p><p>oal. (Image supplied courtesy of Dr. Dwayne Rodgerson).</p><p>igure 10 Sonogram of the abdomen revealing distended fluid-filled</p><p>oops of small intestine typical of small intestinal volvulus. Notice</p><p>he numerous loops of small intestine markedly distended with</p><p>nechoic fluid and the increased amount of peritoneal fluid within</p><p>he abdomen.</p><p>i</p><p>b</p><p>u</p><p>v</p><p>f</p><p>C</p><p>C</p><p>r</p><p>a</p><p>u</p><p>m</p><p>t</p><p>t</p><p>f</p><p>p</p><p>t</p><p>i</p><p>f</p><p>s</p><p>m</p><p>t</p><p>p</p><p>d</p><p>fi</p><p>i</p><p>n</p><p>m</p><p>m</p><p>t</p><p>s</p><p>i</p><p>a</p><p>i</p><p>i</p><p>m</p><p>p</p><p>o</p><p>l</p><p>c</p><p>a</p><p>p</p><p>D</p><p>D</p><p>c</p><p>p</p><p>c</p><p>a</p><p>g</p><p>c</p><p>c</p><p>o</p><p>e</p><p>s</p><p>a</p><p>P</p><p>L</p><p>f</p><p>t</p><p>f</p><p>b</p><p>c</p><p>T</p><p>a</p><p>t</p><p>c</p><p>c</p><p>t</p><p>a</p><p>o</p><p>b</p><p>s</p><p>F</p><p>a</p><p>(</p><p>a</p><p>g</p><p>o</p><p>F</p><p>s</p><p>314 S.B. McAuliffe</p><p>tis/duodenitis. Bacterial and viral infections and hypoxic</p><p>owel syndrome are most common in neonates. Duodenal</p><p>lceration, bacterial (including Lawsonia intracellularis) and</p><p>iral infections, and sand enteritis are more common in older</p><p>oals.</p><p>lostridial Enteritis</p><p>lostridial entercolitis in foals has received much attention in</p><p>ecent years.37,38 Clostridium difficile infection is commonly</p><p>ssociated with nosocomial infections and prior antibiotic</p><p>se. It is, however, thought that C. difficile may act as a pri-</p><p>ary pathogen in foals. Diarrhea and fatal necrotizing en-</p><p>erocolitis have been reported to occur in foals infected with</p><p>oxigenic strains of C. difficile. Clinical presentation may vary</p><p>rom mild diarrhea to profuse diarrhea with colic, tachypnea,</p><p>yrexia, metabolic acidosis, hypoproteinemia, and hypona-</p><p>remia. Diagnosis is based on the detection of C. difficile tox-</p><p>ns in the feces, and a number of tests are now available.</p><p>Clostridium perfringens is a ubiquitous bacterium that is</p><p>ound in the gastrointestinal tract of nearly all warm-blooded</p><p>pecies. Its pathogenesis is based on the production of one or</p><p>ore of the four major recognized exotoxins and/or an en-</p><p>erotoxin. Clinical presentation is usually of a severely de-</p><p>ressed foal �5 days of age with a history of colic and/or</p><p>iarrhea for �24 hours. Enterocolitis and ileus are frequent</p><p>ndings. Specific diagnosis requires the identification of tox-</p><p>ns or toxin genes and isolation of the organism from intesti-</p><p>al contents. However, neonatal C. perfringens is considered a</p><p>edical emergency and a presumptive diagnosis is made in</p><p>any cases by identification of abundant Gram-positive bac-</p><p>eria in a fecal smear, despite the fact that this is not a highly</p><p>ensitive test. Ultrasound findings are variable but commonly</p><p>nclude colitis and/or enteritis with thickened intestinal walls</p><p>nd a fluid-filled lumen. Ileus with an associated decrease in</p><p>ntestinal motility is also common. Gas echoes may also be</p><p>maged in the wall of the affected intestine and is more com-</p><p>igure 11 Sonogram of the right side of the abdomen obtained from</p><p>foal with duodenitis. Notice the mild thickening of the duodenum</p><p>arrow) which was hypomotile in real-time. The adjacent liver also</p><p>ppears more echogenic than normal. The right side of the sono-</p><p>ram is dorsal and the left side is ventral. (Image supplied courtesy</p><p>f Dr. Virginia B. Reef.)</p><p>on with C. perfringens type C infection and is considered a w</p><p>oor prognostic indicator. The identification of such gas ech-</p><p>es or a diphtheritic membrane sloughing into the intestinal</p><p>umen should raise suspicion of Clostridial infection. Many</p><p>ases of neonatal clostridiosis will also have peritonitis, with</p><p>large volume of peritoneal fluid also being regarded</p><p>as a</p><p>oor prognostic indicator.</p><p>uodenitis</p><p>uodenitis frequently accompanies enteritis regardless of the</p><p>ause. Inflammation, erosion, and ulceration affecting the</p><p>ylorus and/or duodenum can impair gastric emptying and</p><p>ause pseudoobstruction.39 Thickening of the duodenal walls</p><p>nd distention of the duodenal lumen are frequent sono-</p><p>raphic findings (Fig. 11). Fibrosis resulting from severe ul-</p><p>eration may lead to pyloric or duodenal strictures. Such</p><p>ases demonstrate gastric distention and there may be a lack</p><p>f normal duodenal motility evident during the sonographic</p><p>xamination. Large amounts of ingesta, persisting in the</p><p>tomach of a fasted or refluxed foal, indicate gastric outflow</p><p>bnormalities.</p><p>roliferative Enteropathy</p><p>awsonia intracellularis causes a proliferative enteropathy in</p><p>oals and other species.40 Most cases are seen in foals from 4</p><p>o 7 months of age, but the disease has been recognized in</p><p>oals as young as 10 days of age.41 Clinical signs are variable</p><p>ut frequently include depression, weight loss, diarrhea,</p><p>olic, and edema (intermandibular edema is most common).</p><p>he progression and severity of the disease are also variable</p><p>nd concurrent infections are frequent findings. Hypopro-</p><p>einemia (�5 g/dL) is the most frequent but inconsistent</p><p>linical pathology finding. Antemortem diagnosis is based on</p><p>linical signs, clinical pathology, exclusion of other condi-</p><p>ions, and the ultrasonographic detection of thickened edem-</p><p>tous segments of small intestine (Fig. 12). Detection of the</p><p>rganism using polymerase chain reaction (PCR) is possible</p><p>ut has low sensitivity. Serological diagnosis is possible, but</p><p>ensitivity and specificity have yet to be determined.</p><p>igure 12 Sonogram of the abdomen obtained from a foal with Law-</p><p>onia intracellularis demonstrating thickened (2.57 cm) edematous</p><p>all of the small intestine.</p><p>A</p><p>A</p><p>R</p><p>o</p><p>o</p><p>o</p><p>a</p><p>i</p><p>S</p><p>I</p><p>f</p><p>b</p><p>e</p><p>T</p><p>fl</p><p>i</p><p>i</p><p>c</p><p>p</p><p>i</p><p>e</p><p>A</p><p>U</p><p>a</p><p>w</p><p>l</p><p>a</p><p>m</p><p>a</p><p>M</p><p>M</p><p>s</p><p>b</p><p>M</p><p>f</p><p>r</p><p>L</p><p>O</p><p>t</p><p>U</p><p>a</p><p>p</p><p>h</p><p>t</p><p>e</p><p>O</p><p>L</p><p>F</p><p>a</p><p>a</p><p>F</p><p>d</p><p>t</p><p>F</p><p>t</p><p>m</p><p>t</p><p>R</p><p>Abdominal ultrasonography of the foal 315</p><p>bdominal Abscesses</p><p>bdominal abscesses in foals are commonly associated with</p><p>hodococcus equi or Streptococcus equi infections. Unilocular</p><p>r multilocular abscesses can be seen and are often imaged at</p><p>r near the ventral abdominal wall, when the weight and size</p><p>f the abscess cause it to displace ventrally (Fig. 13). Such</p><p>bscesses often have extensive adhesions to small and large</p><p>ntestine when identified (Fig. 14).</p><p>and Enteritis/Colitis</p><p>ngestion of sand is common in foals in the Middle East and</p><p>requently results in enteritis and/or colitis. Affected foals can</p><p>e as young as 1 week of age, and the sand is imaged as</p><p>chogenic particles within the stomach and small intestine.</p><p>hickening of the walls of the small intestine and increased</p><p>uidity of intestinal contents is seen with more chronic sand</p><p>ngestion. Occasionally, larger accumulations of sand can be</p><p>igure 13 Sonogram of the abdomen obtained from a foal with an</p><p>bdominal abscess. This is a large (5.53 � 5.61 cm) unilocular</p><p>bscess typical of R. equi abdominal abscesses in foals.</p><p>igure 14 Post mortem picture of a R. equi abdominal abscess in a foal</p><p>emonstrating extensive adhesions to regional small and large in-</p><p>aestine. (Image supplied courtesy of Dr. Fairfield T. Bain.)</p><p>maged in older foals and are generally found in the large</p><p>olon and imaged from the ventral abdomen. Ultrasonogra-</p><p>hy is useful in monitoring large sand accumulations follow-</p><p>ng initial radiography and ultrasonography to determine the</p><p>xtent of the accumulation.42</p><p>scites/Peritonitis</p><p>ltrasonography can be used to evaluate quantity and char-</p><p>cter of peritoneal fluid. Increasing echogenicity correlates</p><p>ith increasing cellularity of the fluid. Anechoic fluid is most</p><p>ikely related to a transudate, although modified transudates</p><p>nd even exudates can have an anechoic appearance. Ho-</p><p>ogenously echoic or echoic and septated fluid is most likely</p><p>n exudate.</p><p>econium Impaction</p><p>econium impactions are readily diagnosed with ultra-</p><p>onography. Meconium is normally imaged as an echogenic</p><p>all or log-shaped structure within the terminal small colon.</p><p>econium in the large colon has a more variable appearance</p><p>rom large hypoechoic to echogenic masses and is often sur-</p><p>ounded by fluid (Fig. 15).1</p><p>arge Intestine Obstruction</p><p>bstruction of the large and small colon with fecaliths or</p><p>richophytobezoars has been infrequently reported in foals.</p><p>ltrasonographic imaging of the mass depends on the</p><p>mount of gas distention of the surrounding intestine. Hy-</p><p>erechoic intralumenal masses casting acoustic shadows</p><p>ave been imaged in foals with bezoars (Fig. 16). Fecaliths in</p><p>he small colon have been successfully imaged and appear as</p><p>chogenic to hyperechoic masses that cast acoustic shadows.1</p><p>ther Large Intestine Disorders</p><p>arge colon displacements or torsions are uncommon in foals</p><p>igure 15 Sonogram of the abdomen of a foal with meconium reten-</p><p>ion in the large intestine. Notice the hypoechoic appearance of the</p><p>econium (arrow) surrounded by the more echoic milky ingesta in</p><p>he foal’s large colon. (Image supplied courtesy of Dr. Virginia B.</p><p>eef.)</p><p>nd are difficult to diagnose ultrasonographically. The gas-</p><p>fi</p><p>b</p><p>c</p><p>d</p><p>d</p><p>a</p><p>R</p><p>1</p><p>1</p><p>1</p><p>1</p><p>1</p><p>1</p><p>1</p><p>1</p><p>1</p><p>1</p><p>2</p><p>2</p><p>2</p><p>2</p><p>2</p><p>2</p><p>2</p><p>2</p><p>2</p><p>2</p><p>3</p><p>3</p><p>3</p><p>3</p><p>3</p><p>3</p><p>3</p><p>3</p><p>3</p><p>3</p><p>4</p><p>4</p><p>4</p><p>F</p><p>1</p><p>h</p><p>(</p><p>t</p><p>316 S.B. McAuliffe</p><p>lled mucosal surface of the large intestine adjacent to the</p><p>ody wall is generally all that can be imaged.1 Thickening,</p><p>ongestion, or edema of the bowel wall may occasionally be</p><p>etected. Persistent abdominal pain accompanied by gaseous</p><p>istention of the large bowel should prompt consideration of</p><p>large colon torsion or displacement.</p><p>eferences</p><p>1. Reef VB: Pediatric abdominal ultrasonography, in Reef (ed): Equine</p><p>Diagnostic Ultrasound. Philadelphia, PA, Saunders, 1998, pp 364-403</p><p>2. Reimer JM: The gastrointestinal tract: the foal, in Reimer (ed): Atlas of</p><p>Equine Ultrasonography. St. Louis, MO, Mosby, 1998, pp 200-211</p><p>3. Reimer JM: Sonographic evaluation of gastrointestinal diseases in foals.</p><p>Proc Am Assoc Equine Pract 39:245-246, 1993</p><p>4. Byars TD, Halley J: Uses of ultrasound in equine internal medicine. Vet</p><p>Clin North Am Equine Pract 2:253-258, 1986</p><p>5. Aleman M, Gillis CL, Nieto JE, et al: Ultrasonographic anatomy and</p><p>biometric analysis of the thoracic and abdominal organs in healthy foals</p><p>from birth to age six months. Equine Vet J 34:649-655, 2002</p><p>6. Reef VB: Ultrasonographic evaluation and diagnosis of foal diseases, in</p><p>Robinson NE (ed): Current Therapy in Equine Medicine III. Philadel-</p><p>phia, PA, Saunders, 1991, pp 417-421</p><p>7. Reef VB, Collatos CA: Ultrasonography of the umbilical structures in</p><p>clinically normal foals. Am J Vet Res 49:2143-2146, 1988</p><p>8. Reef VB, Collatos C, Spencer PA, et al: Clinical, ultrasonographic, and</p><p>surgical findings in foals with umbilical remnant infections. J Am Vet</p><p>Med Assoc 195:69-72, 1989</p><p>9. Hyman SS, Wilkins PA, Palmer JE, et al: Clostridium perfringens ura-</p><p>chitis and uroperitoneum in 2 neonatal foals. J Vet Intern Med 16:489-</p><p>493, 2002</p><p>0. Kablack KA, Embertson RM, Bernard WV, et al: Uroperitoneum in the</p><p>hospitalized equine neonate: retrospective study of 3 cases, 1988-1997.</p><p>Equine Vet J 32:505-508, 2000</p><p>1. Jean D, Marcooux M, Louf CF: Congenital bilateral distal defect of the</p><p>ureters in a foal. Equine Vet Educ 10:17-20, 1998</p><p>2. Lavoie JP, Harnagal SH: Nonsurgical management of ruptured bladder</p><p>in a critically ill foal. J Am Vet Med Assoc 192:1577-1580, 1988</p><p>3. Hoffman KL, Wood AK, McCarthy PH: Ultrasonography of the equine</p><p>neonatal kidney. Equine Vet J 32:109-113, 2000</p><p>4. Andrews FM, Rosol TJ, Kohn CW, et al: Bilateral renal hypoplasia in</p><p>four young horses. J Am Vet Med Assoc 189:209-212, 1986</p><p>5. Gull T, Schmitz DG, Bahr A, et al: Renal hypoplasia and dysplasia in an</p><p>American miniature foal. Vet Rec 149:199-203, 2001</p><p>igure 16 Sonogram of the right side of the abdomen obtained in the</p><p>4th intercostal space of an obstructing bezoar (arrow). Notice the</p><p>yperechoic intralumenal mass casting a strong acoustic shadow</p><p>bezoar) obstructing the intestine in this foal. (Image</p><p>supplied cour-</p><p>esy of Dr. Virginia B. Reef.)</p><p>6. Ramirez S, Williams J, Seahorn TL, et al: Ultrasound assisted diagnosis</p><p>of renal dysplasia in a 3-month old Quarter horse colt. Vet Radiol</p><p>Ultrasound 39:143-146, 1998</p><p>7. Schott HC 2nd, Barbee DD, Hines MT, et al: Clinical vignette. Renal</p><p>arteriovenous malformation in a quarter horse foal. J Vet Intern Med</p><p>10:204-206, 1996</p><p>8. Tomlinson JE, Farnsworth K, Sage AM, et al: Percutaneous ultrasound-</p><p>guided pyelography aided diagnosis of ectopic ureter and hydrone-</p><p>phrosis in a 3-week-old filly. Vet Radiol Ultrasound 42:349-351, 2001</p><p>9. Rantanen NW: Diseases of the kidneys. Vet Clin North Am Equine</p><p>Pract 2:89-103, 1986</p><p>0. Alwaidh MH, Cooke RW, Judd BA: Renal blood flow velocity in acute</p><p>renal failure following cardiopulmonary bypass surgery. Acta Paediatr</p><p>87:644-649, 1998</p><p>1. Wong SN, Lo RN, Yu EC: Renal blood flow pattern by non invasive</p><p>Doppler ultrasound in normal children and acute renal failure patients.</p><p>J Ultrasound Med 8:135-141, 1989</p><p>2. Leveille R, Miyabayashi T, Weisbrode SE, et al: Ultrasonographic renal</p><p>changes associated with phenylbutazone administration in three foals.</p><p>Can Vet J 37:235-236, 1996</p><p>3. Reimer JM: The liver and spleen, in Reimer JM (ed): Atlas of Equine</p><p>Ultrasonography. St. Louis, MO, Mosby, 1998, p 224</p><p>4. Fortier LA: Hepatic diseases in foals, in Mair T, Divers T, Ducharme N</p><p>(eds): Manual of Gastroenterology. Philadelphia, PA, Saunders, 2002,</p><p>pp 513-526</p><p>5. Fortier LA, Fubini SL, Flanders JA, et al: The diagnosis and surgical</p><p>correction of congenital portosystemic vascular anomalies in two calves</p><p>and two foals. Vet Surg 25:154-160, 1996</p><p>6. Santilli RA, Gerboni G: Diagnostic imaging of congenital porto-sys-</p><p>temic shunts in dogs and cats: a review. Vet J 166:7-18, 2003</p><p>7. Divers T: Tyzzer’s disease, in Robinson NE (ed): Current Therapy in</p><p>Equine Medicine IV. Philadelphia, PA, Saunders, 1997, pp 218-219</p><p>8. Traub-Dagartz J, Bayly W, Riggs M, et al: Exsanguination due to gastric</p><p>ulceration in a foal. J Am Vet Med Assoc 186:280-281, 1985</p><p>9. Penninck D, Matz M, Tidwell A: Ultrasonography of gastric ulceration</p><p>in the dog. Vet Radiol Ultrasound 38:308-312, 1997</p><p>0. Wallstabe L, Veitt R, Korner T: Diagnosis of perforated gastric ulcers by</p><p>ultrasound. Z Gastroenterol 40:877-880, 2002</p><p>1. Orsini J: Small intestinal diseases associated with colic in the foal, in</p><p>Mair T, Divers T, Ducharme N (eds): Manual of Gastroenterology.</p><p>Philadelphia, PA, Saunders, 2002, pp 477-484</p><p>2. Cohen ND, Chaffin MK: Intestinal obstruction and other causes of</p><p>abdominal pain in foals. Compend Contin Educ 16:188-195, 1994</p><p>3. Cohen ND, Chaffin MK: Assessment and initial management of colic in</p><p>foals. Compend Contin Educ 17:93-101, 1995</p><p>4. Hanquinet S, Anooshiravani M, Vunda A, et al: Reliability of color</p><p>Doppler and power Doppler sonography in the evaluation of intussus-</p><p>cepted bowel viability. Pediatr Surg Int 13:360-362, 1998</p><p>5. Freeman DE, Orsini JA, Harrison IW, et al: Complications of umbilical</p><p>hernias in horses: 13 cases (1972-1986). J Am Vet Med Assoc 192:804-</p><p>807, 1988</p><p>6. Bernard WV, Reef VB, Reimer JM, et al: Ultrasonographic diagnosis of</p><p>small intestinal intussusception in three foals. J Am Vet Med Assoc</p><p>194:395-397, 1989</p><p>7. Slovis NM: Gastrointestinal failure. Clin Tech Equine Pract 2:79-86,</p><p>2003</p><p>8. Mac Kay RJ: Equine neonatal clostridiosis: treatment and prevention.</p><p>Compend Contin Educ 23:280-283, 2001</p><p>9. Murray MJ: Stomach diseases of the foal, in Mair T, Divers T, Ducharme</p><p>N (eds): Manual of Equine Gastroenterology. Philadelphia, PA, Saun-</p><p>ders, 2002, pp 469-476</p><p>0. Lavoie JP, Drolet R, Parsons D, et al: Equine proliferative enteropathy:</p><p>a cause of weight loss, colic, diarrhea and hypoproteinemia in foals on</p><p>three breeding farms in Canada. Equine Vet J 32:418-425, 2000</p><p>1. Bain FT: Personal communication</p><p>2. Korolainen R, Kaikkonen R, Ruohoniemi M: Ultrasonography in mon-</p><p>itoring the resolution of intestinal sand accumulations in the horse.</p><p>Equine Vet Educ 15:331-336, 2003</p><p>Abdominal Ultrasonography of the Foal</p><p>Scanning Technique</p><p>Umbilical Remnants</p><p>Umbilical Remnant Hemorrhage</p><p>Patent Urachus and Urachal Diverticulum</p><p>Urinary Bladder</p><p>Kidneys</p><p>Liver</p><p>Spleen</p><p>Gastrointestinal Viscera</p><p>Stomach</p><p>Small Intestinal Disorders</p><p>Scrotal/Inguinal Hernias</p><p>Umbilical Hernia</p><p>Intussusception</p><p>Small Intestinal Volvulus/Obstruction</p><p>Ileus</p><p>Enteritis</p><p>Clostridial Enteritis</p><p>Duodenitis</p><p>Proliferative Enteropathy</p><p>Abdominal Abscesses</p><p>Sand Enteritis/Colitis</p><p>Ascites/Peritonitis</p><p>Meconium Impaction</p><p>Large Intestine Obstruction</p><p>Other Large Intestine Disorders</p><p>References</p>