Peter R. Morresey Rood and Riddle Equine Hospital, Lexington, KY, USA Abdominal discomfort in the post foaling mare may result from normal uterine contractions or be indicative of visceral compromise. The uterus and associated structures may be affected or non-reproductive viscera may be involved. Fever, inappetence, and development of generalized sepsis may be the result of disruption of blood supply, contusion, laceration, necrosis, and perforation of either the intestinal and genital tracts. Transabdominal ultrasonography allows non-invasive assessment of peritoneal fluid quantity and quality, visceral disposition, and gives clues as to visceral integrity. Transrectal ultrasonography, when appropriate, improves identification and evaluation of structures distinguished by palpation per rectum. A lower frequency transducer (3.5 MHz or similar) is preferred in larger horses as penetration of the ultrasound beam is enhanced. Smaller horses and foals can be adequately imaged with higher-frequency probes. Clipping of the abdomen with the use of ultrasound coupling gel may give the best image; but in practical settings, wetting with alcohol and slicking down hair in the direction of growth to expel air is sufficient. Clipping of a suitable acoustic window may be unavoidable in horses with matted or seasonally long hair coats. The probe is then held perpendicular to the abdominal wall and then systematically moved in a dorsal-ventral direction and, when along the midline, cranial-caudal. The more cranial aspects of the abdominal cavity are located within the thoracic rib cage and imaging of this area uses a similar technique to that detailed for thoracic ultrasonography. Examination of the left side of the horse reveals the liver applied medially to the diaphragm and ventrally to the lung fields variably between the seventh to ninth intercostal spaces (ICS) [1]. The liver is lateral to the spleen in this region, with the stomach visualized deep to this interface; however, the stomach may have variable contact with the body wall depending on degree of fill. The spleen is imaged over the majority of the left side of the abdominal cavity medial to the body wall from the paralumbar fossa to the eighth ICS, and further cranially medial to the liver as noted above. The spleen extends ventrally to the midline and may extend to the right ventral abdomen. Spleen size is variable. The left kidney lies medial to the spleen and is found from the sixteenth ICS through the paralumbar fossa. Gas filled viscera may obstruct complete visualization of the left kidney. Examination of the right side of the abdominal cavity reveals liver variably from the sixth to the fifteenth ICS medially and lung and diaphragm ventrally [1]. The right kidney is located dorsally and superficially in the same region, adjacent to the caudal most aspects of the liver in the fourteenth to seventeenth ICS region. The intestinal tract is imaged via the caudal and ventral abdomen. The small intestine is variable in location and can be seen on the left, right, and often both sides of the abdomen. Ventral colon is applied to the ventral abdominal wall and identified by sacculations (haustra). The liver is not imaged from the ventral abdomen in the normal horse [1]. The right dorsal colon can be seen applied to the liver medially on the right side. The cecum is noted in the right paralumbar fossa traversing caudally and ventrally before the cecal tip trends cranially. The bladder, when urine filled, is located on the ventral midline of the caudal abdomen. The non-pregnant uterus is not discernible in the absence of pathology. Varying stages of pregnancy and uterine pathology can be noted, depending on uterine size and disposition. Portions of the intestinal tract (jejunum) may be noted lateral to the spleen on the left side, with some appearing dorsal and lateral to the dorsal most aspect of the spleen. In the absence of colonic content trapped in the nephrosplenic space, this does not appear to cause problems. Peritoneal fluid can often be imaged accumulated dorsal to the spleen. The limitations of transabdominal ultrasonography are a result of the size of the abdominal cavity relative to the penetrating ability of the ultrasound transducer which depends on the nominal frequency. Gas shadowing is commonplace and can obscure deeper structures from view. The anatomy of the horse provides a challenge as a considerable proportion of the abdominal cavity lies within the caudal rib cage. Discontinuities of the abdominal wall are present, with alterations of the expected contour. Subcutaneous edema, pockets of fluid, hemorrhage, and muscle fiber disruption are visible with ultrasonography (Figure 28.1). Diagnosis of the specific tissue involved can be difficult [2]. Abdominal wall ruptures laterally tend to occur at the junction of the rectus abdominis and oblique muscles. Muscle layers tend to tear along their fiber direction. Rupture of the peritoneum allows intestine to directly appose the subcutaneous musculature or skin. Prepubic tendon rupture results in ventral abdominal wall deviation, elevation of the tailhead, regional edema, and pain cranial to the mammary gland [2]. Herniation of intestine through abdominal wall tears has the potential to result in incarcerated intestine [2]. Large tears may allow colon to herniate, while extensive amounts of jejunum can herniate through small tears. Diaphragmatic hernia is a rare parturient complication [3] and can also be found in athletic horses. Viscera reported to be involved in diaphragatic hernias include small intestine, large intestine, stomach, spleen, and liver [4,5]. The colon appears as a thick-walled, sacculated structure with fluid and gas content. The small intestine appears as multiple, tubular fluid-filled structures. If structures are no longer contained within the peritoneum (hernial sac), a diaphragmatic rupture has occurred. With ultrasonography, intrathoracic intestine may be visualized appearing cranial to the diaphragm and shadowing the lung due to gaseous content. Pleural fluid may be increased. Strangulation of intestine may result in visualization of thickened intestinal wall and increased peritoneal and pleural fluid (Figure 28.2). An intraluminal air-fluid interface may be present [6]. Prognosis is considered guarded. One review involving variable horse signalments found a survival rate in diagnosed cases of diaphragmatic hernia to be 23%. This increased to 46% survival rate following surgical correction [4]. Perirenal hemorrhage may occur secondary to renal pathology, or from direct trauma to the kidney itself. Blunt force trauma sustained during prolonged dystocia may induce perirenal hemorrhage (Figure 28.3). Transrectal ultrasonography may detect fluid or fibrin caudal to the peritoneal reflection (Figure 28.4). Caudal vaginal or rectal trauma during parturition may be sufficient to cause hemorrhage, tissue necrosis, sepsis, or perforation. This may not be reflected in grossly observable changes in the adjacent peritoneal cavity. Changes in the peritoneal fluid reflect the altered integrity of the viscera within the peritoneum. These include ultrasonographically detectable changes in peritoneal fluid amount, echogenicity, and sometimes disposition. Increase in value of two or more fluid variables, including total protein, nucleated cell count, and percentage neutrophils, is considered significant [7]. Periparturient hemorrhage can develop in mares of any age or parity; however, it is more common in older mares [8–10]. While the genital tract is the most likely source in the periparturient mare, examination of the liver, spleen, and kidneys is prudent. Mesenteric disruption can also lead to hemoperitoneum. Hemoperitoneum has a characteristic ultrasonographic appearance in the initial stages of hemmorhage. The fluid appears cellular and swirling (smoke-like) in response to diaphragmatic and visceral movements (Figure 28.5). Appearance will vary with rate of formation, volume of hemorrhage, and duration of bleed. With time, clot formation occurs ventrally, with relatively anechoic fluid remaining dorsally (Figure 28.6). Hemorrhage may be acute and overwhelming, intermittent and repeated, or chronic and persistent at low levels. Peritonitis (Figure 28.7) may result when intestinal bruising, strangulation, and ischemia progress to mural necrosis and rupture of the affected intestinal segment. The condition may progress over a number of days, with abdominal discomfort and fever preceding overt signs of sepsis. This results from progressive bacterial translocation across devitalized intestine or uterine wall. Spillage of gastrointestinal content precipitates a rapid onset of systemic deterioration. Peritonitis has also been reported secondary to bladder wall necrosis [11]. Peritoneal fluid appears echogenic, cellular to flocculent to turbid, and may in advanced cases contain fibrin strands free or attached to regional peritoneal (visceral and parietal) surfaces (Figure 28.8). Volume of peritoneal fluid may be highly variable: small in acute or dehydrated patients and large where spillage of intestinal or uterine content has occurred. Gas echoes or highly echogenic particles are consistent with a ruptured viscus. Mesenteric abscess formation may result in chronic cases (Figure 28.9). The urine-filled bladder may routinely be imaged in the inguinal region via the transabdominal or transrectal routes. The bladder content and wall dimensions give clues as to ongoing inflammatory and/or infectious processes (Figure 28.10). The bladder wall may become traumatized and devitalized by compression against the pelvic brim. This pressure may be sufficient to cause rupture (Figure 28.11) during parturition [12
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Post Foaling Complications
Introduction
Technique
Normal Anatomy
Common Variations
Limitations of Transabdominal Ultrasonography
Pathology of the Abdominal Boundaries
Ruptured Body Wall, Ruptured Rectus Abdominis, and Prepubic Tendon
Diaphragmatic Hernia
Retroperitoneal Hemorrhage (Perirenal)
Pelvicitis
Pathology of the Peritoneal Cavity
Hemoperitoneum
Peritonitis
Cystitis, Uroperitoneum, and Bladder Rupture
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