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Abdominal Ultrasonography of the Foal

Siobhan B. McAuliffe, MVB


Disorders of abdominal organs represent a large proportion of diseases encountered in equine neonatal medicine. Ultrasonography was rst used in the equine neonate for the diagnosis of internal umbilical remnant infections and has since been used for the diagnosis of a wide variety of disorders. Ultrasound is noninvasive, well tolerated by the foal, and easily performed in the eld. In addition, the smaller size of the foal abdomen and proximity of many organs of interest makes the foal an ideal candidate for abdominal ultrasonography. These factors have led to increasing use of ultrasonography in the equine neonate; with this increased use has come awareness of the prognostic as well as diagnostic features of ultrasound. This article reviews the technique for abdominal ultrasonography, including its advantages and limitations, and provides an overview of necessary equipment. The ultrasonographic appearance of abdominal organs under normal and pathologic conditions is also described. Clin Tech Equine Pract 3:308-316 2004 Elsevier Inc. All rights reserved. KEYWORDS ultrasonography, neonate, abdominal, renal, umbilical, hepatic

Scanning Technique

Umbilical Remnants
The umbilical vein is located along the midline from the external umbilicus to the liver and becomes the round ligament of the liver. It is a small oval or elliptical vessel with a thin echogenic wall and an anechoic center. The umbilical vein usually measures 10 mm or less in diameter throughout its length.7 The umbilical arteries course caudally from the external umbilical remnant and become the round ligaments of the bladder. They are thick walled with a diameter of 12 mm or less and commonly contain an echogenic clot. The urachus retracts after birth and becomes the median ligament of the bladder. In the normal foal, it contains no uid. Umbilical remnant infections may be external (Fig. 1), internal, or both and have frequently been incriminated as a source of septicemic infections.8 External infections may be detected clinically in the presence of heat, pain, swelling, or discharging purulent material or can be diagnosed ultrasonographically as an enlarged thickened external umbilical remnant containing hypoechoic to echogenic uid.8 Hyperechoic echoes representing gas may be detected and are indicative of an anaerobic infection if there is no gas-lled tract extending from the skin surface into the external umbilical remnant.9 Internal infections are best diagnosed with ultrasonography. Enlargement of any of the internal remnant structures, with the detection of intraluminal uid, indicates the presence of infection. Involvement of multiple structures is common in foals with internal umbilical remnant infection.1,2,8 Infection of the urachus and umbilical arteries is most common, with less frequent involvement of the umbilical vein.8 The infected umbilical vein is enlarged ( 10 mm) with the most prominent enlargement at or near the external

ltrasonographic examination of the abdominal organs has been well described in foals.1-6 Sector and linear transducers can be used, and both produce high-quality images. Sector scanners have a small footprint that facilitates intercostal imaging. Linear transducers produce a rectangular image that is well suited for examining supercial structures; however, with increasing depth, the image of the far eld is narrowed which restricts visualization of deep structures. Curved linear transducers provide wide near and far elds of view, and the footprint size is usually intermediate. The highest frequency transducer that penetrates to the area of interest should be used and the smallest depth of eld necessary should be displayed. Sedation is not generally required but may be necessary in certain individuals. For optimal image quality, the entire ventral abdomen should be clipped with a #40 surgical clipper blade from the xiphoid caudally to the inguinal region. The lateral abdomen and paralumbar fossa should also be clipped ventral to a line drawn from the tuber coxae to the elbow. Ultrasound coupling gel should be applied following washing of the abdomen with warm water. Examination of the gastrointestinal viscera is performed from the most ventral location to avoid interference from gas present in the gastrointestinal viscera that rises dorsally.

The Stables of HRH Crown Prince Abdullah bin Abdul Aziz & Sons, Riyadh. Address reprint requests and correspondence to: Siobhan B. McAuliffe, MVB, The Stables of HRH Crown Prince Abdullah bin Abdul Aziz & Sons, PO Box 46935, Riyadh, Kingdom of Saudi Arabia, 11542. E-mail: siobhanmcauliffe@hotmail.com

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1534-7516/04/$-see front matter 2004 Elsevier Inc. All rights reserved. doi:10.1053/j.ctep.2005.02.008

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Figure 1 Enlarged external umbilicus in a foal with an external umbilical remnant infection.

Figure 3 Sonogram of the abdomen from a foal with hemoabdomen. Notice the large amount of echoic uid surrounding the collapsed thickened loops of small intestine (small arrows).

umbilical remnant. The luminal contents can vary from anechoic to echogenic material. Thickening of the walls of the umbilical vein is likely with longstanding infection. Extension cranially into the liver may result in hepatic abscesses or suppurative hepatitis and warrants a thorough sonographic examination of the liver. An infected umbilical artery is enlarged ( 13 mm) with a thickened wall and contains anechoic to echoic uid. Although the greatest increase in diameter of the artery may occur anywhere along its length, the infected umbilical artery is usually largest just caudal to the external umbilical remnant or at the apex of the bladder.1 An infected urachus is enlarged and lled with anechoic, hypoechoic, or echogenic uid (Fig. 2). A combined measurement for the urachus and both umbilical arteries at the apex of the

bladder greater than 25 mm indicates infection.1,8 Longstanding infections may become walled off and appear as encapsulated abscesses. Identication of infection of any of the internal umbilical remnants should be followed by careful examination of adjacent organs.

Umbilical Remnant Hemorrhage


Hemorrhage from the umbilical cord at parturition may result in swelling of the internal umbilical vessels or perivascular tissues. Rupture of the umbilical vein or artery may result in hemoabdomen which is imaged as echogenic swirling uid (Fig. 3) within the peritoneal cavity, or a large area of vascular and perivascular hemorrhage may be imaged with or without a brin clot.1,2 Occasionally, brin clots may be visualized in the bladder or urachus.

Patent Urachus and Urachal Diverticulum


Anechoic uid within the urachus that is continuous with the bladder apex and external umbilicus is indicative of a patent urachus. A urachal diverticulum is a uid-lled caudal urachus continuous with the bladder apex and has been implicated as a cause of stranguria in the foal.2

Urinary Bladder
The bladder is adjacent to the ventral abdominal wall for 4 to 8 weeks after birth; thereafter, the large colon is interspersed between the bladder and ventral abdominal wall. The bladder can still be visualized in the caudoventral and midlateral abdomen in foals up to 6 months of age. Maximal bladder distension in 1- and 7-day-old foals has been reported as 9 and 10 cm, respectively.5 Ultrasound has become extremely useful in detecting uroabdomen associated with defects of the bladder wall or urachus. Uroperitoneum has been recognized in otherwise healthy and hospitalized neonates. Affected foals that are otherwise healthy are most commonly male, less than 1 week old, with a history of stranguria and progressive abdominal distention. These foals typically develop hyponatremia, hy-

Figure 2 Sonogram of the urachus and both umbilical arteries in a foal with urachitis and omphaloarteritis. Notice the enlarged thick walled urachus (large arrows) lled with hypoechoic uid. The umbilical arteries are the small echoic structures with the hyperechoic rim along the endothelium of the vessel. The left umbilical artery (the small arrow to the right) is enlarged and lled with hypoechoic uid, while the right umbilical artery (the small arrow to the left) is normal size but also contains a small amount of hypoechoic uid. This is a transverse sonogram with the right side of the abdomen displayed on the left side of the sonogram. (Image supplied courtesy of Dr. Virginia B. Reef.)

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important as nonsurgical treatment of urachal and ureteral defects may be successful. Medical treatment of a bladder wall defect in a critically ill foal has also been reported, but these defects generally require surgical intervention.12

Kidneys
The right kidney is located ventral to the transverse spinous processes between the 14th and 16th intercostal spaces (ICS) from 2 cm dorsal to the tuber coxae to 12 cm ventral. The right kidney has a heart-shaped appearance. The left kidney has a bean-shaped appearance and is located from the 15th ICS to the caudal border of the left paralumbar fossa and from 2 cm dorsal to 15 cm ventral to the dorsal margin of the tuber coxae. Measurement of kidney length and width in foals up to 6 months of age showed a signicant difference between right and left kidneys, with the left kidney being longer and the right kidney being wider for all age groups.5 The renal pelvis and calices are hyperechoic, the renal cortex is hypoechoic in relation to the renal calices, and the renal medullary pyramids are relatively anechoic, allowing for a prominent corticomedullary junction. The renal capsule is imaged as a thin hyperechoic line surrounding the kidney. As in mature horses, the echogenicity of the renal cortex is less than that of the liver, which in turn is less than that of the spleen.13 Congenital renal defects that may be detected by ultrasound include renal cysts, renal hypoplasia, renal dysplasia, renal agenesis, renal arteriovenous malformation, and ectopic ureters. Measurements of renal length and width for foals up to 6 months of age have been reported, with continual growth of both kidneys in that time frame.5 Renal hypoplasia is recognized as a smaller than normal kidney and can be unilateral or bilateral.14 Renal dysplasia is recognized ultrasonographically as misshapen, hyperechoic kidneys with decreased corticomedullary demarcation.15,16 Renal agenesis should be considered when a kidney cannot be found in a normal or ectopic location. In humans and small animals, the

Figure 4 Sonogram of the abdomen from a foal with uroperitoneum. Notice the large amount of anechoic uid in the abdominal cavity and the loops of jejunum (arrows) oating within the uid. (Image supplied courtesy of Dr. Virginia B. Reef.)

pochloremia, hyperkalemia, and azotemia. Hospitalized patients that developed uroperitoneum showed no signicant gender predilection in one study, and there was a signicant relationship between sepsis and uroperitoneum.10 In these patients, the development of the disorder is postulated to have two etiologies: one is ischemia and necrosis of the bladder wall and the other is manipulation of obtunded patients with distended bladders. The clinical chemistry ndings are less consistent in this group and may be related to earlier recognition in hospitalized patients or concurrent uid therapy for other disorders. In addition to the noninvasive nature of the procedure, ultrasonography is useful in locating the site of the defect for surgical repair, with a signicant relationship existing between the ultrasound ndings and lesion location at surgical exploration.10 The most common defect is in the dorsal bladder wall. Defects of the ureters are less common, and congenital causes of uroabdomen have also been reported.11 The ultrasound image obtained shows free peritoneal uid (Fig. 4). The volume and character of the uid vary depending on the time course involved: small amounts of anechoic uid in recent onset uroabdomen to large amounts of hypoechoic uid with brin strands if secondary peritonitis exists. The gastrointestinal viscera are seen oating in the abdominal uid (Fig. 4), and the urinary bladder can also be imaged oating in the uid. Depending on the size and location of the defect, the bladder may contain anechoic urine or be collapsed and folded on itself (Fig. 5). This folding of the bladder wall is characteristic of a bladder wall defect and should not be confused with a recently voided bladder, which has a small contracted appearance but does not appear folded. Defects in the urachus result in dissection of uid into the surrounding tissues, and the bladder usually has a round and uid-lled appearance, as the defects are generally small and result in slow leakage of urine into the peritoneal cavity. Foals which have a normal appearance of both the bladder and urachal remnants with uroperitoneum are likely to have a ureteral defect.6 The ureters are not normally visible, and thus direct imaging of the defect with ultrasonography is not possible. Attempts to identify the location of the defect are

Figure 5 Sonogram of the bladder obtained transcutaneously from the ventral abdomen of a foal with a ruptured bladder. Notice the folded appearance of the ruptured bladder oating in the surrounding anechoic uid. The defect in the dorsal wall of the bladder is not clearly visible but is adjacent to the tip of the arrow. In real-time, uid was imaged passing through this defect. (Image supplied courtesy of Dr. Virginia B. Reef.)

Abdominal ultrasonography of the foal


contralateral kidney hypertrophies with time. Renal arteriovenous malformation has been recognized in a Quarter Horse. Color ow Doppler ultrasonography demonstrated an anomalous vascular connection between artery and vein of the affected kidney.17 Direct imaging of ectopic ureters is not normally possible but ultrasound guided pyelography has been used to diagnose ectopic ureters.18 Renal disease is relatively common in neonatal foals associated with peripartum asphyxia and hypoxic renal injury. However, ultrasound evaluation of the kidneys in these foals has not demonstrated consistent ndings. Enlarged kidneys that are less echogenic than normal and consistent with acute renal failure have been seen in some foals; while in other foals, there have been no abnormalities detected or only a slight increase in parenchymal echogenicity.1,4,19 Recently, assessment of renal blood ow as an indication of acute renal failure in foals has become more commonplace in large referral institutions, but to date there has been no controlled study of its prognostic value. Children with acute renal failure have an absence of blood ow in late diastole or throughout diastole that is easily detected with Doppler ultrasound.20,21 Renal failure secondary to the administration of nephrotoxic drugs is also of great importance in foals. Development of a diffuse hyperechoic zone in the renal medulla near the corticomedullary junction has been reported in two of three foals administered phenylbutazone at 5 mg/kg body weight for 7 days. These foals did not demonstrate clinical signs of renal failure, and the ultrasound changes were correlated to mineralization in the collecting tubules of the medullary region. The potential clinical signicance of these changes was not determined.22

311 multifocal abscessation with an ultrasonographic appearance of multiple small areas of increased echogenicity scattered throughout the hepatic parenchyma.1 Hepatic abscesses, although rare in foals, can occur secondary to ascending umbilical vein infections or as a progression of a suppurative hepatitis.8 When detected early, these abscesses are hypoechoic with ill dened margins; as they progress and become surrounded by more echogenic inammatory tissue, they become better dened.1 Portal vein thrombosis has been reported in calves with hepatic abscessation and in one foal with an umbilical abscess, Streptococcus zooepidemicus cellulitis and pneumonia, and Rhodococcus equi polyarthritis and pneumonia.24 In this case, the hepatic parenchyma appeared normal ultrasonographically with a thrombus occupying 90% of the portal vein, as well as the primary intrahepatic portal vein branches. Treatment consisted of antibiotics and antiinammatory drugs. Repeat ultrasound examinations demonstrated a recannulization of the portal vein and the development of hyperechogenic foci in the liver parenchyma. With the thrombus resolved, the liver enzymes, which had initially been elevated, declined, and despite the presence of abnormal echogenic foci in the liver, no permanent hepatic function abnormalities were detected.24 Cholangiohepatitis has been reported in foals as a sequela of gastroduodenal ulceration.24 Duodenal strictures occurring secondary to gastroduodenal ulceration can lead to cholangiohepatitis through two mechanisms. If the stricture develops at the hepaticoduodenal area, bile duct obstruction and ascending cholangiohepatitis can follow. Strictures that occur aborad to the bile duct can result in bile stasis and reux of ingesta into the bile duct with ascending infection. Thickening of the bile ducts with echogenic material imaged within the biliary tree is indicative of cholangiohepatitis.1,6

Liver
The liver can normally be seen in the cranioventral and midabdomen between the 7th and 14th ICS and dorsally in the 14th ICS on the right side of the abdomen. On the left side, it can be seen between the 6th and 10th ventrolateral ICS in a larger area compared with mature animals.5 Hepatic vessels can be seen diffusely throughout the liver parenchyma. The walls of the portal veins are more echogenic than the hepatic veins as they are surrounded by more connective tissue.23 Portosystemic shunts are anomalies of the portosystemic circulation that allow direct communication between the portal circulation and a systemic vein such as the vena cava. These anomalies are rare in horses, and diagnosis is based on history, clinical signs, clinical pathology, and contrast portography.24,25 Doppler ultrasonography may be a useful diagnostic aid and has commonly been used in dogs for the detection of extrahepatic shunts.26 Intrahepatic shunts and other vascular anomalies are more difcult to detect. Tyzzers disease in foals is an acute bacterial hepatitis, myocarditis, and /or colitis and has been reported in foals from 7 to 92 days of age. Ante-mortem diagnosis is difcult as there is no rapid denitive diagnostic test. It should be suspected in any foal with acute hepatic failure, hepatic enlargement, and a diffuse increase in parenchymal echogenicity.27 Septicemia in foals may result in bacterial hepatitis via hematogenous inoculation. Many species of bacteria have been incriminated, but Actinobacillus equuli in particular has been associated with hepatitis and nephritis, characterized by

Spleen
The spleen is imaged between the 7th ICS and the paralumbar fossa (PLF) on the left side and in the 9th ventral ICS on the right side in contact with the liver. The splenic vein is imaged on the medial aspect of the spleen, caudal and dorsal to the stomach in the 11th to 12th mid-ICS. The spleen interfaces caudally with the left kidney and is homogenously echogenic, with few vessels seen.5 Splenic abnormalities are rare in foals. Trauma resulting in a splenic hematoma and/or hemoabdomen may occur.

Gastrointestinal Viscera
The clinical signs of abdominal visceral disease may be mild, such as decreased nursing or lethargy, and can be difcult to distinguish from signs associated with other neonatal disorders. Abdominal disorders are common in the neonatal period, and thorough evaluation of the gastrointestinal tract should be performed in all foals with signs referable to the gastrointestinal tract or in those with nonspecic signs. Due to their small size and proximity of many organs of interest, neonatal foals are ideal candidates for ultrasonographic evaluation of the viscera.

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Stomach
The stomach is located medial to the spleen in the mid- to ventral abdomen between the 6th and 12th ICS on the left side. The ventral wall of the stomach is in contact with the ventral abdomen up to 7 days of age.5 The stomach wall is hypoechoic relative to surrounding structures. In foals less than 7 days, luminal contents are visible. In older foals, the presence of gas prevents imaging of the gastric contents, and at this stage, the foals stomach resembles that of an adult with a large curvilinear echo medial to the spleen and caudal to the liver. Ultrasonographic examination of the stomach is an essential part of sonographic examination of the abdomen in foals with suspected abdominal disease. Distention of the stomach may be pronounced and easily detected with small intestinal obstructions. Gastric and duodenal distention is commonly seen in foals with gastroduodenal ulcers. Gastric rupture may occur secondary to gastric ulceration or obstructive disorders. A marked increase in peritoneal uid is noted on sonographic examination in foals with a ruptured viscus. The character of the uid is highly variable and depends on the age of the foal (predominantly milk diet) and the duration of the rupture. Exsanguination with a resultant hemoabdomen secondary to gastric ulceration has also been reported.28 Ultrasonography has also been used in dogs and humans to detect gastric ulceration, with or without perforation.29,30 The small intestine can be visualized in a larger area of the abdomen in young foals compared with adults. The small intestine has a hypoechoic wall and its lumen is easily observed. The duodenum is visualized between the ventral and caudal aspect of the liver and the dorsal margin of the right dorsal colon. It can also be seen ventral to the caudal pole of the right kidney and dorsal to the cecal base.5 The large intestine is recognized by its larger diameter and sacculated appearance. The lumen of the large intestine is not normally visualized due to the presence of gas.

Figure 6 Sonogram of the abdomen obtained from a foal with a nonreducible umbilical hernia. There is an incarcerated loop of small intestine present within the umbilical hernia. Notice the thickened edematous wall of the small intestine and the surrounding peritoneal uid within the hernial sac.

Small Intestinal Disorders


Small intestinal disorders are common in foals and range from congenital defects, such as scrotal/inguinal hernias and Meckels diverticulum, to enteritis, ascarid impaction, volvulus, intussusception, or abdominal abscesses.31-33

Scrotal/Inguinal Hernias
Inguinal hernias are generally noticed within a few days of birth as soft uctuant swellings in the inguinal region and scrotum. The hernia can be easily reduced when the foal is rolled onto its back. Scrotal hernias in foals usually resolve spontaneously and incarceration of intestine in the hernia is rare. Ultrasonography can be used to characterize the viability of incarcerated bowel in these rare instances; with compromised bowel having a thickened and edematous wall and decreased to absent peristaltic movement. Color ow Doppler can also be used to assess the blood ow of the incarcerated segment.34

an incidence of 0.5% to 2%.30 The majority of umbilical hernias are small ( 2.5 cm in diameter) and are easily reduced. Ultrasonography is used in addition to digital palpation to determine the size of the defect. The contents of the hernial sac (uid, omentum, or intestine) and the presence of concurrent internal umbilical or subcutaneous infection can also be assessed ultrasonographically. Determining the size of the defect by measuring the diameter in a sagittal and transverse plane aids in selecting the most appropriate procedure for closure. The uncomplicated umbilical hernia appears as a defect in the ventral abdominal wall, whereas a complicated umbilical hernia also has infection of the internal or external umbilical remnants or adjacent subcutaneous structures. Nonreducible umbilical hernias can occur with strangulation or incarceration of omentum, small intestine, ventral colon, or cecum within the hernial sac. Strangulation should be suspected in a nonreducible hernia that increases in size, warmth, and becomes painful, hot, and edematous. Such foals often present with or have a history of colic, but the severity of pain is not a reliable indicator of strangulation or other complications.35 Fat contained within the omentum gives a heterogeneous hypoechoic to echogenic appearance. Strangulated ileum (most common) or jejunum has a thickened, edematous wall with decreased or absent motility (Figs. 6 and 7).1 Color ow Doppler can also be used to assess bowel viability in such cases.34 If large bowel is involved, only a portion of the ventral colon or cecum is incarcerated within the hernia and is imaged as an outpouching of the large intestine with thickened, edematous, and amotile walls.

Intussusception
The use of ultrasound to detect intussusceptions in foals is well reported with a characteristic bulls eye or target sign being obtained by scanning through the apex of the intussusception where the intussusceptum is surrounded by uid and the intussuscipiens (Figs. 8 and 9).1,2,36 Different sono-

Umbilical Hernia
Umbilical hernias are the second most common congenital defect in horses (cryptorchidism is the most common) with

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Figure 7 Intraoperative picture of the incarcerated small intestine from the foal in Figure 6. Note the thickened edematous bowel wall and congestion of the associated blood vessels.

Figure 9 Intraoperative picture of an ileo-ileal intussusception in a foal. (Image supplied courtesy of Dr. Dwayne Rodgerson).

thickened, amotile intestine proximal to and in the area of the obstruction.

graphic appearances may be obtained depending on the portion of the intussusception being imaged. Jejunojejunal intussusceptions are most common in young foals and have been linked to bacterial and protozoal infections, and the use of prokinetic drugs. Ileo-ileal and ileo-cecal intussusceptions can also be seen in older foals, weanlings, and yearlings.

Ileus
Sonographic examination of foals with ileus usually reveals bowel with an increased diameter and little if any peristaltic activity.1,2 The intestinal wall thickness is usually normal but may be increased with certain etiologies, and other intestinal or peritoneal uid abnormalities may be detected. Mechanical ileus associated with intussusceptions, volvulus, obstructive embryonic remnants, mural masses, meconium or ascarid impactions, and trichophytobezoars produces segmental dilation; whereas functional ileus associated with hypoxic bowel injury, surgery, or anesthesia produces generalized distention.

Small Intestinal Volvulus/Obstruction


Fluid-lled, amotile small intestine with thicker than normal walls is suggestive of a small intestine volvulus (Fig. 10). The degree of wall thickness increases with the passage of the time and the wall may be of normal thickness soon after the volvulus occurs making differentiation from ileus difcult. Volvulus is most often seen in foals less than 3 months of age and may affect the entire small intestine or only a small portion. Pain is severe and the clinical condition of these foals rapidly deteriorates. Meckels diverticulum and other embryologic remnants may cause small intestine obstruction resulting in

Enteritis
The sonographic appearance of enteritis is variable, but uidlled hypermotile bowel is usually present. Intestinal wall thickness is also variable but is generally symmetric. Many etiologies have been implicated in the development of enter-

Figure 8 Sonogram of the abdomen obtained from a foal with a small intestinal intussusception. Notice the target or bulls eye appearance of the small intestinal intussusception (arrow). Three different portions of the intussusception are depicted in sonographic image.

Figure 10 Sonogram of the abdomen revealing distended uid-lled loops of small intestine typical of small intestinal volvulus. Notice the numerous loops of small intestine markedly distended with anechoic uid and the increased amount of peritoneal uid within the abdomen.

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poor prognostic indicator. The identication of such gas echoes or a diphtheritic membrane sloughing into the intestinal lumen should raise suspicion of Clostridial infection. Many cases of neonatal clostridiosis will also have peritonitis, with a large volume of peritoneal uid also being regarded as a poor prognostic indicator.

Duodenitis
Duodenitis frequently accompanies enteritis regardless of the cause. Inammation, erosion, and ulceration affecting the pylorus and/or duodenum can impair gastric emptying and cause pseudoobstruction.39 Thickening of the duodenal walls and distention of the duodenal lumen are frequent sonographic ndings (Fig. 11). Fibrosis resulting from severe ulceration may lead to pyloric or duodenal strictures. Such cases demonstrate gastric distention and there may be a lack of normal duodenal motility evident during the sonographic examination. Large amounts of ingesta, persisting in the stomach of a fasted or reuxed foal, indicate gastric outow abnormalities.

Figure 11 Sonogram of the right side of the abdomen obtained from a foal with duodenitis. Notice the mild thickening of the duodenum (arrow) which was hypomotile in real-time. The adjacent liver also appears more echogenic than normal. The right side of the sonogram is dorsal and the left side is ventral. (Image supplied courtesy of Dr. Virginia B. Reef.)

itis/duodenitis. Bacterial and viral infections and hypoxic bowel syndrome are most common in neonates. Duodenal ulceration, bacterial (including Lawsonia intracellularis) and viral infections, and sand enteritis are more common in older foals.

Proliferative Enteropathy
Lawsonia intracellularis causes a proliferative enteropathy in foals and other species.40 Most cases are seen in foals from 4 to 7 months of age, but the disease has been recognized in foals as young as 10 days of age.41 Clinical signs are variable but frequently include depression, weight loss, diarrhea, colic, and edema (intermandibular edema is most common). The progression and severity of the disease are also variable and concurrent infections are frequent ndings. Hypoproteinemia ( 5 g/dL) is the most frequent but inconsistent clinical pathology nding. Antemortem diagnosis is based on clinical signs, clinical pathology, exclusion of other conditions, and the ultrasonographic detection of thickened edematous segments of small intestine (Fig. 12). Detection of the organism using polymerase chain reaction (PCR) is possible but has low sensitivity. Serological diagnosis is possible, but sensitivity and specicity have yet to be determined.

Clostridial Enteritis
Clostridial entercolitis in foals has received much attention in recent years.37,38 Clostridium difcile infection is commonly associated with nosocomial infections and prior antibiotic use. It is, however, thought that C. difcile may act as a primary pathogen in foals. Diarrhea and fatal necrotizing enterocolitis have been reported to occur in foals infected with toxigenic strains of C. difcile. Clinical presentation may vary from mild diarrhea to profuse diarrhea with colic, tachypnea, pyrexia, metabolic acidosis, hypoproteinemia, and hyponatremia. Diagnosis is based on the detection of C. difcile toxins in the feces, and a number of tests are now available. Clostridium perfringens is a ubiquitous bacterium that is found in the gastrointestinal tract of nearly all warm-blooded species. Its pathogenesis is based on the production of one or more of the four major recognized exotoxins and/or an enterotoxin. Clinical presentation is usually of a severely depressed foal 5 days of age with a history of colic and/or diarrhea for 24 hours. Enterocolitis and ileus are frequent ndings. Specic diagnosis requires the identication of toxins or toxin genes and isolation of the organism from intestinal contents. However, neonatal C. perfringens is considered a medical emergency and a presumptive diagnosis is made in many cases by identication of abundant Gram-positive bacteria in a fecal smear, despite the fact that this is not a highly sensitive test. Ultrasound ndings are variable but commonly include colitis and/or enteritis with thickened intestinal walls and a uid-lled lumen. Ileus with an associated decrease in intestinal motility is also common. Gas echoes may also be imaged in the wall of the affected intestine and is more common with C. perfringens type C infection and is considered a

Figure 12 Sonogram of the abdomen obtained from a foal with Lawsonia intracellularis demonstrating thickened (2.57 cm) edematous wall of the small intestine.

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Figure 13 Sonogram of the abdomen obtained from a foal with an abdominal abscess. This is a large (5.53 5.61 cm) unilocular abscess typical of R. equi abdominal abscesses in foals.

Figure 15 Sonogram of the abdomen of a foal with meconium retention in the large intestine. Notice the hypoechoic appearance of the meconium (arrow) surrounded by the more echoic milky ingesta in the foals large colon. (Image supplied courtesy of Dr. Virginia B. Reef.)

Abdominal Abscesses
Abdominal abscesses in foals are commonly associated with Rhodococcus equi or Streptococcus equi infections. Unilocular or multilocular abscesses can be seen and are often imaged at or near the ventral abdominal wall, when the weight and size of the abscess cause it to displace ventrally (Fig. 13). Such abscesses often have extensive adhesions to small and large intestine when identied (Fig. 14).

imaged in older foals and are generally found in the large colon and imaged from the ventral abdomen. Ultrasonography is useful in monitoring large sand accumulations following initial radiography and ultrasonography to determine the extent of the accumulation.42

Ascites/Peritonitis
Ultrasonography can be used to evaluate quantity and character of peritoneal uid. Increasing echogenicity correlates with increasing cellularity of the uid. Anechoic uid is most likely related to a transudate, although modied transudates and even exudates can have an anechoic appearance. Homogenously echoic or echoic and septated uid is most likely an exudate.

Sand Enteritis/Colitis
Ingestion of sand is common in foals in the Middle East and frequently results in enteritis and/or colitis. Affected foals can be as young as 1 week of age, and the sand is imaged as echogenic particles within the stomach and small intestine. Thickening of the walls of the small intestine and increased uidity of intestinal contents is seen with more chronic sand ingestion. Occasionally, larger accumulations of sand can be

Meconium Impaction
Meconium impactions are readily diagnosed with ultrasonography. Meconium is normally imaged as an echogenic ball or log-shaped structure within the terminal small colon. Meconium in the large colon has a more variable appearance from large hypoechoic to echogenic masses and is often surrounded by uid (Fig. 15).1

Large Intestine Obstruction


Obstruction of the large and small colon with fecaliths or trichophytobezoars has been infrequently reported in foals. Ultrasonographic imaging of the mass depends on the amount of gas distention of the surrounding intestine. Hyperechoic intralumenal masses casting acoustic shadows have been imaged in foals with bezoars (Fig. 16). Fecaliths in the small colon have been successfully imaged and appear as echogenic to hyperechoic masses that cast acoustic shadows.1

Figure 14 Post mortem picture of a R. equi abdominal abscess in a foal demonstrating extensive adhesions to regional small and large intestine. (Image supplied courtesy of Dr. Faireld T. Bain.)

Other Large Intestine Disorders


Large colon displacements or torsions are uncommon in foals and are difcult to diagnose ultrasonographically. The gas-

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of renal dysplasia in a 3-month old Quarter horse colt. Vet Radiol Ultrasound 39:143-146, 1998 Schott HC 2nd, Barbee DD, Hines MT, et al: Clinical vignette. Renal arteriovenous malformation in a quarter horse foal. J Vet Intern Med 10:204-206, 1996 Tomlinson JE, Farnsworth K, Sage AM, et al: Percutaneous ultrasoundguided pyelography aided diagnosis of ectopic ureter and hydronephrosis in a 3-week-old lly. Vet Radiol Ultrasound 42:349-351, 2001 Rantanen NW: Diseases of the kidneys. Vet Clin North Am Equine Pract 2:89-103, 1986 Alwaidh MH, Cooke RW, Judd BA: Renal blood ow velocity in acute renal failure following cardiopulmonary bypass surgery. Acta Paediatr 87:644-649, 1998 Wong SN, Lo RN, Yu EC: Renal blood ow pattern by non invasive Doppler ultrasound in normal children and acute renal failure patients. J Ultrasound Med 8:135-141, 1989 Leveille R, Miyabayashi T, Weisbrode SE, et al: Ultrasonographic renal changes associated with phenylbutazone administration in three foals. Can Vet J 37:235-236, 1996 Reimer JM: The liver and spleen, in Reimer JM (ed): Atlas of Equine Ultrasonography. St. Louis, MO, Mosby, 1998, p 224 Fortier LA: Hepatic diseases in foals, in Mair T, Divers T, Ducharme N (eds): Manual of Gastroenterology. Philadelphia, PA, Saunders, 2002, pp 513-526 Fortier LA, Fubini SL, Flanders JA, et al: The diagnosis and surgical correction of congenital portosystemic vascular anomalies in two calves and two foals. Vet Surg 25:154-160, 1996 Santilli RA, Gerboni G: Diagnostic imaging of congenital porto-systemic shunts in dogs and cats: a review. Vet J 166:7-18, 2003 Divers T: Tyzzers disease, in Robinson NE (ed): Current Therapy in Equine Medicine IV. Philadelphia, PA, Saunders, 1997, pp 218-219 Traub-Dagartz J, Bayly W, Riggs M, et al: Exsanguination due to gastric ulceration in a foal. J Am Vet Med Assoc 186:280-281, 1985 Penninck D, Matz M, Tidwell A: Ultrasonography of gastric ulceration in the dog. Vet Radiol Ultrasound 38:308-312, 1997 Wallstabe L, Veitt R, Korner T: Diagnosis of perforated gastric ulcers by ultrasound. Z Gastroenterol 40:877-880, 2002 Orsini J: Small intestinal diseases associated with colic in the foal, in Mair T, Divers T, Ducharme N (eds): Manual of Gastroenterology. Philadelphia, PA, Saunders, 2002, pp 477-484 Cohen ND, Chafn MK: Intestinal obstruction and other causes of abdominal pain in foals. Compend Contin Educ 16:188-195, 1994 Cohen ND, Chafn MK: Assessment and initial management of colic in foals. Compend Contin Educ 17:93-101, 1995 Hanquinet S, Anooshiravani M, Vunda A, et al: Reliability of color Doppler and power Doppler sonography in the evaluation of intussuscepted bowel viability. Pediatr Surg Int 13:360-362, 1998 Freeman DE, Orsini JA, Harrison IW, et al: Complications of umbilical hernias in horses: 13 cases (1972-1986). J Am Vet Med Assoc 192:804807, 1988 Bernard WV, Reef VB, Reimer JM, et al: Ultrasonographic diagnosis of small intestinal intussusception in three foals. J Am Vet Med Assoc 194:395-397, 1989 Slovis NM: Gastrointestinal failure. Clin Tech Equine Pract 2:79-86, 2003 Mac Kay RJ: Equine neonatal clostridiosis: treatment and prevention. Compend Contin Educ 23:280-283, 2001 Murray MJ: Stomach diseases of the foal, in Mair T, Divers T, Ducharme N (eds): Manual of Equine Gastroenterology. Philadelphia, PA, Saunders, 2002, pp 469-476 Lavoie JP, Drolet R, Parsons D, et al: Equine proliferative enteropathy: a cause of weight loss, colic, diarrhea and hypoproteinemia in foals on three breeding farms in Canada. Equine Vet J 32:418-425, 2000 Bain FT: Personal communication Korolainen R, Kaikkonen R, Ruohoniemi M: Ultrasonography in monitoring the resolution of intestinal sand accumulations in the horse. Equine Vet Educ 15:331-336, 2003

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Figure 16 Sonogram of the right side of the abdomen obtained in the 14th intercostal space of an obstructing bezoar (arrow). Notice the hyperechoic intralumenal mass casting a strong acoustic shadow (bezoar) obstructing the intestine in this foal. (Image supplied courtesy of Dr. Virginia B. Reef.)

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lled mucosal surface of the large intestine adjacent to the body wall is generally all that can be imaged.1 Thickening, congestion, or edema of the bowel wall may occasionally be detected. Persistent abdominal pain accompanied by gaseous distention of the large bowel should prompt consideration of a large colon torsion or displacement.

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References
1. Reef VB: Pediatric abdominal ultrasonography, in Reef (ed): Equine Diagnostic Ultrasound. Philadelphia, PA, Saunders, 1998, pp 364-403 2. Reimer JM: The gastrointestinal tract: the foal, in Reimer (ed): Atlas of Equine Ultrasonography. St. Louis, MO, Mosby, 1998, pp 200-211 3. Reimer JM: Sonographic evaluation of gastrointestinal diseases in foals. Proc Am Assoc Equine Pract 39:245-246, 1993 4. Byars TD, Halley J: Uses of ultrasound in equine internal medicine. Vet Clin North Am Equine Pract 2:253-258, 1986 5. Aleman M, Gillis CL, Nieto JE, et al: Ultrasonographic anatomy and biometric analysis of the thoracic and abdominal organs in healthy foals from birth to age six months. Equine Vet J 34:649-655, 2002 6. Reef VB: Ultrasonographic evaluation and diagnosis of foal diseases, in Robinson NE (ed): Current Therapy in Equine Medicine III. Philadelphia, PA, Saunders, 1991, pp 417-421 7. Reef VB, Collatos CA: Ultrasonography of the umbilical structures in clinically normal foals. Am J Vet Res 49:2143-2146, 1988 8. Reef VB, Collatos C, Spencer PA, et al: Clinical, ultrasonographic, and surgical ndings in foals with umbilical remnant infections. J Am Vet Med Assoc 195:69-72, 1989 9. Hyman SS, Wilkins PA, Palmer JE, et al: Clostridium perfringens urachitis and uroperitoneum in 2 neonatal foals. J Vet Intern Med 16:489493, 2002 10. Kablack KA, Embertson RM, Bernard WV, et al: Uroperitoneum in the hospitalized equine neonate: retrospective study of 3 cases, 1988-1997. Equine Vet J 32:505-508, 2000 11. Jean D, Marcooux M, Louf CF: Congenital bilateral distal defect of the ureters in a foal. Equine Vet Educ 10:17-20, 1998 12. Lavoie JP, Harnagal SH: Nonsurgical management of ruptured bladder in a critically ill foal. J Am Vet Med Assoc 192:1577-1580, 1988 13. Hoffman KL, Wood AK, McCarthy PH: Ultrasonography of the equine neonatal kidney. Equine Vet J 32:109-113, 2000 14. Andrews FM, Rosol TJ, Kohn CW, et al: Bilateral renal hypoplasia in four young horses. J Am Vet Med Assoc 189:209-212, 1986 15. Gull T, Schmitz DG, Bahr A, et al: Renal hypoplasia and dysplasia in an American miniature foal. Vet Rec 149:199-203, 2001 16. Ramirez S, Williams J, Seahorn TL, et al: Ultrasound assisted diagnosis

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37. 38. 39.

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