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Uroperitoneum in the Equine Neonate
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Introduction
Uroperitoneum has been recognized as a syndrome in foals for over 50 years [1,2]. Traditionally, it has been thought to present most frequently in the 24 - 36 hour old male foal during the post-parturient period [2-4]. Previous reports had a proportionately larger affected male than female population [2,3,5]. It was hypothesized that colts were more at risk due to their long narrow high resistance urethra that was less likely to allow bladder emptying, resulting in rupture of a full bladder during parturition when high pressures were applied focally or circumferentially around the bladder [1,6-8].
Rupture or disruption of any structure of the urinary tract can occur. Of the case studies reviewed, 8 of 16 foals with an identified site of rupture in one study, and 24 of 31 foals in another, had a bladder defect [4,9]. The dorsal wall of the bladder has been reported to be a frequent disruption site, with the ventral wall less likely to be involved [4,6,9]. The urachus appears to be the next most commonly affected structure. A few cases of ureteral and urethral defects have been reported [4,5]. Sepsis does not appear to favor one site over the others [9].
Pathophysiology
The exact pathophysiology of uroperitoneum is not fully understood. It was once thought that high pressures exerted on a full bladder during parturition was the main cause [1,2,6-8]. Others proposed that a full bladder and obstruction due to a partial umbilical cord torsion may be a cause of rupture during parturition [6,11]. Strenuous exercise and external trauma have also been seen as causes [6,9-11]. The lesions associated with the above causes typically have inflamed and hemorrhagic edges, consistent with trauma. A few reports exist where possible congenital bladder wall defects were proposed due to the smooth and non-inflamed edges of the tissue [6,10,12]. These claims, however, are disputed. Recently, more focus has been put focal infection and sepsis as factors leading to urinary tract rupture and uroperitoneum. Adams and Koterba [4] showed an association between septicemia, urinary tract infections and rupture of the urinary tract. This finding was supported by Kablack, et.al. In a retrospective study of 31 cases of uroperitoneum they found a relationship between neonatal illness and the development of uroperitoneum [9].
Clinical Signs
Clinical signs associated with uroperitoneum in the neonatal foal typically include straining to urinate, dribbling urine, and a stretched out stance [2]. At this point, the condition is often confused with colic due to meconium impaction of the gastrointestinal tract. Meconium impacted foals, however, usually have a roached back and stand with all four limbs underneath them as they strain to defecate [2,3]. Weakness, tachycardia, tachypnea, and not sucking well are also seen in uroperitoneum [2-4,6,9,14]. As the uroperitoneum progresses and fluid accumulates, a distended abdomen may be observed [2,3]. A fluid wave may be felt on ballottement of the abdomen [3]. Occasionally, scrotal accumulation of urine can occur [15]. With the recognition of sepsis as a contributing factor to the development of uroperitoneum, many foals also show signs of concurrent infection and sepsis, including fever, injected mucous membranes, diarrhea, and diseases of other body systems.
Laboratory Findings
Laboratory findings are variable, depending on the duration of the uroperitoneum as well as the presence and severity of sepsis. However, some classic findings include hyperkalemia, hyponatremia, and hypochloremia [3-5]. These abnormalities arise from the equilibration of urine electrolytes and water with blood across the peritoneal membrane, allowing for loss of sodium and chloride and retention of potassium. The usual foal diet consists of milk that is high in potassium and low in sodium, perpetuating and exacerbating the electrolyte abnormalities. Those cases recognized very early in the clinical course of the disease may not have these classic signs. The time for equilibration of electrolytes and water across the peritoneal surface is not known in the horse, however, cases diagnosed may not have electrolyte abnormalities [9]. Foals who develop uroperitoneum while hospitalized, and receiving intravenous fluids, may not have electrolyte imbalances due to the composition of the administered fluids, which compensate for electrolyte derangements and may mask them [9]. Increased serum creatinine concentration is often present. Serum blood urea nitrogen concentrations are occasionally, but not consistently, increased [3-5]. Metabolic acidosis and hypoxemia may be present. Some patients have also demonstrated serum hypo-osmolality [3]. Foals should have their serum IgG concentration tested, as they may have failure of passive transfer due to weakness and failure to nurse, or have decreased IgG concentration secondary to sepsis. This has been recognized by Kablack et.al and also at our hospital [9]. One of the most sensitive laboratory tests for determination of uroperitoneum is the peritoneal to serum creatinine ratio. A ratio greater than or equal to 2 to 1 is diagnostic for uroperitoneum [3,5,6,13,15,16]. Peritoneal fluid should be collected and tested for creatinine concentration, as well as for cytology, culture and sensitivity. Cytologic evaluation of peritoneal fluid is crucial to identify peritonitis or concurrent gastrointestinal compromise. Cytologic analysis and culture of two foals presenting for uroabdomen at our hospital revealed Clostridium perfringens urachitis and peritonitis. This organism was concurrently isolated from blood cultures of both foals and large gram-positive bacilli were present on histologic examination of the ruptured urachus of one. The second foal also had a ruptured urachus, but was not examined histologically. An electrocardiogram should be performed on initial evaluation of a foal with suspected uroperitoneum. Hyperkalemia may result in bradycardia, increased duration of the QRS complex, a shortened QT interval, increased P-wave duration, prolonged P-R interval, or AV conduction disturbances. Other possible cardiac sequelae to hyperkalemia include cardiac arrest, third degree A-V block, ventricular premature contractions, and ventricular fibrillation [5,6].
Diagnostic Procedures
Many diagnostic procedures exist to help confirm the diagnosis of uroperitoneum. Abdominocentesis with peritoneal to serum creatinine ratio is an easy and accurate test to perform [2,3]. Injection of dyes (methylene blue, red sulfonamide solution) into the bladder via urethral catheterization with subsequent retrieval of dye in the peritoneal fluid has also been used [3,5]. Radiography can be a useful tool for diagnosis of uroperitoneum. Plain films can identify fluid within the abdomen, but usually cannot identify the defect. Contrast studies can help to further delineate the site of the lesion. Positive contrast, double contrast, or a pneumocystogram have all been used. These tests can yield false negative results if an inadequate volume of dye is used and/or the defect is very small and dorsally located [15]. Intravenous pyelography can be used to identify ureteral defects, although results are inconsistent [5,15]. Any foal exhibiting signs of dyspnea, tachypnea and/or hypoxemia should have thoracic radiographs taken prior to induction of anesthesia in order to rule out pleural effusion, pneumonia, or acute respiratory distress syndrome, which could complicate ventilation and oxygenation during anesthesia and the postoperative period. Ultrasonography has become an invaluable tool in the diagnosis of uroperitoneum and is now the most useful tool available to the practitioner [4-6,9,15]. Imaging of free peritoneal fluid, as well as its characteristics (hypocellular, cellular, fibrinous, gas-echoes) can be accomplished. Identification of the urinary tract lesion is also possible. Tears within the bladder are readily seen and the empty bladder in a fluid-filled abdomen will collapse on itself and often have a U-shape [17]. Urachal and urethral lesions can also be visualized. Six of eight foals in one study had urinary tract lesions identified sonographically and all 31 foals of another study underwent sonographic evaluation and a significant (P<0.05) correlation between ultrasonographic findings and location of the lesion at surgery existed [4,9].
Treatment
Uroperitoneum should be treated as a medical emergency. Initial treatment should be directed at stabilizing the patient and correcting any electrolyte and acid-base abnormalities and providing fluid volume replacement. 0.9% or 0.45% saline should be used until laboratory data are available so that additional potassium is not provided to a potentially hyperkalemic patient. This will also help to slowly correct the hyponatremia and hypochloremia. Potassium levels >5.5 mEq/L can be life threatening and should be addressed quickly. The hyperkalemia can be managed by peritoneal drainage to help remove the source of the potassium. This can be performed with teat cannulas, foley catheters, large gauge (16g or 14g) intravenous catheters, or in the author's experience, human peritoneal dialysis catheters work extremely well and are less likely to be fully blocked with omentum and fibrin due to their multiple fenestrations. Fluid replacement should match the amount of fluid removed to prevent acute hypotension due to expansion of previously collapsed capillary beds. Abdominal drainage will also help ventilation and decrease the work of breathing by decreasing pressure on the diaphragm. Serum potassium levels can be decreased preoperatively by this technique. We have been successful with this technique in our hospital. Use of intravenous Ca++ gluconate, glucose, sodium bicarbonate, and insulin will also decrease potassium levels, however, it must be remembered that the potassium has only been driven into the cells and once therapy is discontinued, as total body potassium is still increased, it can once again equilibrate out into the serum causing increased potassium levels. Hyponatremia should also be slowly corrected. The central nervous system maintains its own sodium homeostasis even in the face of whole body depletion. Rapid administration of sodium (i.e. hypertonic saline) can lead to an intracellular influx of sodium and water that can cause cellular edema and neurological signs. If hyponatremia has been of several days duration, rapid correction can result in central pontine lesions, as with time, the brain will adjust intracellular osmolytes to match the extracellular conditions. Blood cultures should be obtained prior to administration of preoperative antimicrobials. Broad-spectrum coverage such as that provided by penicillin and amikacin or ceftiofur sodium is recommended until culture results are available. Aminoglycosides should be used cautiously in foals with decreased renal function and serum peak and trough levels should be monitored. Foals with failure of passive transfer should be treated with adequate volumes of intravenous plasma. Once the metabolic abnormalities have been addressed, surgical management can be considered. Most cases require surgical correction [2-5,9,15]. One case of medical management of a small dorsal tear using an indwelling Foley catheter was described by Lavoie [14]. Often the timing choice for surgical intervention is difficult due to the patient instability and the anesthetic risks associated with the frequently present hyperkalemia and hyponatremia. Most foals are weak, dehydrated, acidotic, and hyperkalemic. However, if the preoperative medical stabilization is properly accomplished, the anesthetic risks can be minimized. The ability to mask down these foals with inhalant anesthesia, as well as safer agents such as isoflurane, decreases risks. Surgical repair techniques have been first described in 1958 by DuPleiss [2]. Since then many other techniques for repair of ruptured bladder have been presented [5,18-20]. Briefly, a midline or paramedian incision is made. The bladder defect is identified and closed with absorbable suture in an inverting pattern making sure to place the sutures in healthy tissue. The abdomen should be lavaged, especially if cytology of peritoneal fluid suggests infection. Urinary catheters and peritoneal drains can be placed on surgeon preference. Body wall and skin closure is routine. It is now usual for the internal umbilical remnant to be removed at the time of surgery. Laparoscopic repair of a bladder defect was successfully performed by Edwards, Ducharme, and Hackett [13], however, the possibility of urolith formation from non-absorbable laparoscopic sutures may be a contraindication for this technique [13]. Repair of other urinary tract defects (ureters,urethras) are described in the literature [18-20].
Complications associated with the primary urinary tract defect as well as those of concurrent disease can occur. Recurrence of the urinary tract rupture can occur. Dysrhythmias from electrolyte abnormalities are commonly seen. Hypotension from hyperkalemia and hypocalcemia may also be present. Other non-urinary tract complications may be just as serious. Sepsis, hypoxemia, pneumonia, peritonitis, and acute respiratory distress syndrome all complicate the management of uroperitoneum. One case was complicated by a hole in the diaphragm that allowed peritoneal fluid into the thorax and caused pulmonary edema [3].
Prognosis
Prognosis is closely associated with concurrent illness, especially septicemia. Uncomplicated uroperitoneum from a defect in the bladder has a good prognosis [2,4,5,9]. If the location of the lesion is other than the bladder, the prognosis is historically not as favorable. Richardson and Kohn reported only 1 of 10 survivors with lesions found in the urachus or ureters [5]. This may have been due to concurrent septicemia, which was not factored into risk factors for survival in that study. Foals with septicemia have a much poorer prognosis. Adams and Koterba reported a 50% long-term survival rate in 18 foals on their study. Seven of the nine non-survivors had bacterial or fungal infections [4]. Kablack, et al. [9] found an association between death and sepsis, increased serum sodium and chloride, decreased potassium, and an increased peritoneal to serum creatinine ratio. The unusual association with normal electrolyte concentrations is likely due to foals being hospitalized for conditions such as sepsis and receiving intravenous fluid therapy.
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1.Bain AM. Disease of foals. Aust. Vet 1954; 30:9-12.
2.Du Plessis JL. Rupture of the bladder in the newborn foal and its surgical correction. J S Afr Vet Assoc 1958; 29:261-263.
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New Bolton Center, School of Veterinary Medicine, University of Pennsylvania, Kennett Square, Pennsylvania, USA.
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