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Phosphate enema toxicosis in a pygmy goat wether Shirani A. Hickman, Marjorie S. Gill, Steven L. Marks, Julie A. Smith, Gary A. Sod Abstract — Phosphate enema toxicity was diagnosed in a 7-month-old, castrated male, pygmy goat. On presentation, clinical findings included mild depression, tachycardia, tachypnea, rumen stasis, muscle tremors, hypocalcemia, hypokalemia, hypochloremia, hyperphosphatemia, azotemia, and metabolic acidosis. Fluid diuresis and parenteral antimicrobial therapy resulted in recovery after 3 d of treatment. Résumé — Toxicose par lavement phosphatique chez un bouc castré pygmée. La toxicité des lavements phosphatiques a été diagnostiquée chez un bouc pygmée castré âgé 7 ans. À la présentation, les trouvailles cliniques comprenaient une dépression légère, de la tachycardie, de la tachypnée, une stase au rumen, des tremblements musculaires, une hypocalcémie, une hypokaliémie, une hypochlorémie, une hyperphosphatémie, une azotémie et une acidose métabolique. Une fluidothérapie et une thérapie antimicrobienne ont conduit à un rétablissement après 3 jours de traitement. (Traduit par Docteur André Blouin) Can Vet J 2004;45:849–851
13.6 kg, 7-month-old, castrated male, pygmy goat A with a history of straining, vocalizing, and no urine or feces production for the previous 2 d was presented
for emergency treatment. There was no history of vaccination or deworming. For 3 d prior to presentation, the goat had been fed 2 cups of cracked corn daily in place of his usual diet of all-purpose livestock feed. Two days prior to admission, food and water intake had decreased, and the owner had noted abdominal distention. Absence of fecal output and continued straining resulted in the owner administering 5 adult (120 mL each) sodium phosphate enemas (Fleet; CB Fleet Company, Lynchburg, Virginia, USA) on the day of presentation, 1 each hour, over a 5-hour period. At presentation, the goat was depressed but responsive. The rectal temperature was 39.4°C (reference range, 38.5 to 40.2°C); heart rate, 144 beats/min (reference range, 70 to 120 beats/min); and respiratory rate, 100 breaths/min (reference range, 10 to 30 breaths/min). The hydration status was determined to be adequate. The abdomen was tense on palpation, the rumen was moderately distended with fluid and gas, and rumen motility was absent. The urinary bladder was not evident on abdominal palpation. The goat’s hind legs were stiff, and fine muscle tremors of the head and neck were noticed. Department of Veterinary Clinical Sciences and Veterinary Teaching Hospital & Clinics, School of Veterinary Medicine, Louisiana State University, Baton Rouge, Louisiana 70803, USA. Dr. Hickman’s current address is 4895 Hwy 84 West, Vidalia, Louisiana 71373, USA. Address all correspondence and reprint requests to Dr. Marjorie S. Gill, e-mail:
[email protected] Can Vet J Volume 45, October 2004
In an attempt to relieve rumen tympany, a nasogastric tube was passed; this resulted in reflux of a small amount of pungent ruminal fluid with a pH of 6.0. Serum biochemical analysis revealed markedly increased blood urea nitrogen (BUN) (16 mmol/L; reference range, 2 to 4.6 mmol/L), creatinine (380 mmol/L; reference range, 79.5 to 159 mmol/L), and phosphorous (7.6 mmol/L; reference range, 1.4 to 3 mmol/L), with hypocalcemia (0.95 mmol/L; reference range, 2.1 to 2.6 mmol/L), hypochloremia (94 mmol/L; reference range, 105 to 120 mmol/L), hypokalemia (3.3 mmol/L; reference range, 4.6 to 6.7 mmol/L), and metabolic acidosis (TCO2, 21.9 mmol/L; reference range, 26 to 30 mmol/L). Marked hypocalcemia, hyperphosphatemia, and metabolic acidosis, in conjunction with the clinical presentation and history, were compatible with phosphate enema overdose, although concurrent renal or postrenal disease could not be ruled out at that time. Because of the possibility of obstructive urolithiasis and ruptured bladder, abdominocentesis was attempted, but fluid collection was unsuccessful. Radiographic and ultrasound imaging were not performed because of financial constraints and lack of after-hours availability. Near the end of the initial examination, the goat passed a small amount of urine making postrenal obstruction less likely. Urinalysis revealed a specific gravity of 1.021 (reference range, 1.001 to 1.050), pH of 8.0 (reference range, 7.2 to 8.0), protein of 3 (reference range, negative to trace), a large amount of hemoglobin (reference range, negative), white blood cells (5 to 10/high-power field [hpf]; reference range, 5/hpf), and a few calcium carbonate crystals (reference range, rare). Treatment was initiated with an IV bolus of 150 mL of lactated Ringer’s solution with added calcium (10 mL of 10% calcium gluconate) over 30 min, shortly after 849
which the goat produced about 30 mL of urine. Broadspectrum antibiotic therapy (procaine penicillin G [Agri-Cillin; AgriLabs, St. Joseph, Missouri, USA], 44 000 U/kg body weight [BW], SC q12h, and ceftiofur sodium [Naxcel; Pharmacia and Upjohn, Kalamazoo, Michigan, USA], 2.2 mg/kg BW, SC q24h) was administered due to concern of possible bacterial translocation from the rectum to the systemic circulation following the multiple enema administrations. Lactated Ringer’s solution was continued at 1.5 times the maintenance rate (56 mL/h) for 12 h. Urine production continued during the fluid administration, although it was not measured at that time. On the following day, the goat’s rectal temperature, heart rate, and respiratory rate were within the reference ranges and he passed approximately 50 mL of urine. Light green, mucoid feces were present on digital rectal examination, and fine tremors of the head and neck were still present. The goat ate small amounts of grass, but no ruminal motility was detected. A 2nd serum biochemical analysis revealed improvement in all previously abnormal parameters: BUN, 10.6 mmol/L; calcium, 1.9 mmol/L; and potassium, 3.5 mmol/L were improved, while creatinine, 159 mmol/L; phosphorous, 2.9 mmol/L; chloride, 111 mmol/L; and TCO2, 26.5 mmol/L were within reference range. Over the next few days of hospitalization, the goat became more alert and responsive, his appetite improved, and feces became more normal in appearance and consistency. His temperature, heart rate, and respiratory rate were within the reference ranges, and no muscle tremors were noted. Lactated Ringer’s solution was continued IV at 56 mL/h and urine production during that time was estimated to be approximately 1 mL/kg BW/h. Intravenous fluids were gradually decreased as free choice water intake increased and administration of parenteral antibiotics was discontinued. The patient was discharged 5 d after admission with the recommendation that he be maintained on a roughage-only diet with free choice water. The diagnosis of sodium phosphate enema toxicity was made based on history, clinical findings, and response to therapy. Other potential complicating factors in this case included indigestion (mild acute rumen acidosis) and possible obstructive urolithiasis, renal disease, or both. The owners of the goat were contacted 12 mo after discharge, and reported that the goat had experienced no more health problems. Adverse effects of sodium phosphate laxatives, in oral or enema preparations, have been reported in the human and veterinary medical literature (1–9). At one time, it was believed that the phosphate in enema preparations was not systemically absorbed, leading to the belief that these enemas were relatively innocuous (1,2) and resulting in injudicious use of these products. Recent studies have confirmed that significant phosphate is absorbed into the systemic circulation through the colon (2,3). In a healthy individual with normal phosphorus intake, the majority of this absorbed phosphorus can be handled via renal excretion or intracellular transfer (4). However, in patients with altered gastrointestinal motility or renal insufficiency, increased intestinal absorption or decreased renal excretion may lead to 850
hyperphosphatemia and subsequent electrolyte abnormalities (1,4–8). The recommended dose range for small animals is 1 adult-sized (120 mL) enema for an animal that weighs 11.3 kg, or more, or 1 pediatric-sized (60 mL) enema for a smaller animal (3,8). Administration of enemas above this dose in healthy animals can result in signs of toxicity. However, even doses within the recommended therapeutic range can cause phosphate enema toxicity (3,8). This has most commonly been described in small animals, such as cats and dogs (3,7,8). Phosphate enema toxicity has not, to our knowledge, been described in ruminant species. Clinical signs observed with phosphate enema toxicity in dogs and cats can appear as early as 30 to 40 min after administration and can include weakness, dehydration, shock, tetany, seizures, and death (3,8). The weakness detected in these cases is thought to be due to hypokalemia. It has been proposed that the dehydration with subsequent hypovolemic shock could be the result of fluid influx into the hypertonic contents of the colon (3,8). The tetany seen is usually caused by hypocalcemia. The combination of fluid and electrolyte imbalances can result in seizures and death. Common biochemical abnormalities described with phosphate enema toxicity in humans, cats, and pigs include hyperphosphatemia, hypocalcemia, and metabolic acidosis (1–7,9). The hyperphosphatemia is a result of the absorption of phosphate from the colon. Decreased intestinal motility and subsequent constipation can enhance this absorption (1,4). The absorption can also be increased by any mucosal damage present in the distal intestinal tract (7). Additionally, increases in intracellular phosphate concentration leads to an intracellular movement of calcium, further decreasing serum calcium levels (7). Different theories have been proposed for the mechanism by which metabolic acidosis occurs in phosphate enema toxicity. Calcium-hydrogen ion exchange at the level of the cellular membrane and lactic acidosis has been suggested as a possible mechanism (2). The pathogenesis of acidosis may also involve dysfunction of the phosphate-dependent portion of cellular metabolism (1,4). Hypernatremia resulting from the sodium content in the enema was another commonly noted abnormality in humans and cats (2,4,7). Hypokalemia, present in several studies, was presumably a result of excessive potassium loss through excretion in feces or urine (7). Hypomagnesemia was present in at least one case study in a human patient with chronic renal insufficiency (6). Hyperglycemia was noted in 2 studies involving cats (3,7). Azotemia was an uncommon finding in previous studies (3). The possible causes for the increases in BUN and creatinine in this case were renal and postrenal. It has been reported that hyperphosphatemia may have nephrotoxic effects in cats (3). Diuresis is the most important component of the treatment of phosphate enema toxicity. Intravenous fluid administration increases total body fluids, thereby promoting renal phosphate excretion. Isotonic fluids such as lactated Ringer’s solution are acceptable for treatment of phosphate enema toxicity, but electrolyte-poor solutions, such as 5% dextrose in water or 0.45% sodium Can Vet J Volume 45, October 2004
chloride, are usually recommended (7). Isotonic saline (0.9% sodium chloride) should be avoided in patients with hypernatremia because of its high sodium content; it may also worsen hypocalcemia by promoting calciuresis (7,9). Calcium gluconate can be added to fluids, but fluid expansion alone may normalize serum calcium levels. Systemic antimicrobials may be useful in preventing sepsis when the integrity of the colonic mucosa is in question (7). The integrity of the intestinal mucosa can be compromised by the presence of any ulcerative intestinal disease, constipation, tenesmus, and repeated enema use, so antibiotics could be useful in treating and preventing systemic infections resulting from bacterial translocation across damaged mucosa. Overdosage played a major role in the toxicity of the enemas in this case. One adult phosphate enema contains 118 mL of a sodium phosphate solution, 161 mg/mL of monobasic sodium phosphate, and 59 mg/mL of dibasic sodium phosphate (10). An experimental study performed on pigs showed that the enema solution was lethal if retained in doses above 20 mL/kg BW (2). The goat in this case received a total of 590 mL, which, if retained, is equivalent to a 43 mL/kg BW dose, more than twice the lethal dose in pigs. The amount of enema solution actually retained in this case was unknown. Fortunately, the dose was not fatal in this case. Possible reasons for survival include timely treatment of the problem, phosphorus metabolism differences between
goats and pigs, or both. Research has shown that ruminants metabolize dietary phosphorus differently from nonruminants, but adequate information comparing ruminant to nonruminant colonic absorption and metabolism of phosphorus is not available (11). In this case, multiple factors may have contributed to the adverse effects following the phosphate enemas. Indigestion secondary to grain engorgement may have resulted in rumen atony and tympany, which decreased gastrointestinal motility. This, in turn, could have contributed to an increase in intestinal absorption of phosphate. Failure of the goat to defecate following the multiple enemas may have led to prolonged enema retention and further increased intestinal absorption. Although never confirmed, a lower urinary tract obstruction was suspected initially, based on straining and the lack of urine output noticed 2 d before presentation; however, if partial or complete urethral obstruction was present, it had resolved prior to presentation. The azotemia may have been a result of postrenal obstruction. This goat had a clinical history typical of urinary or intestinal tract obstruction. In either event, enema administration was probably not an appropriate treatment, since conditions requiring enema administration in the goat are rare. This case is an example of injudicious use of sodium phosphate enemas that signals the necessity for thorough examination of the patient to determine the need for enema administration. In the event that an enema is required, a safer product, such as dioctyl CVJ sodium succinate, may be indicated.
References 1. Helikson MA, Parham WA, Tobias JD. Hypocalcemia and hyperphosphatemia after phosphate enema use in a child. J Pediatr Surg 1997;32:1244–1246. 2. Martin RR, Lisehora GR, Braxton M Jr, Barcia PJ. Fatal poisoning from sodium phosphate enema. Case report and experimental study. J Am Med Assoc 1987;257:2190–2192. 3. Atkins CE, Tyler R, Greenlee P. Clinical, biochemical, acid-base, and electrolyte abnormalities in cats after hypertonic sodium phosphate enema administration. Am J Vet Res 1985;46: 980–988. 4. Fass R, Do S, Hixson LJ. Fatal hyperphosphatemia following Fleet phospho-soda in a patient with colonic ileus. Ann J Gastroenterol 1993;88:929–932. 5. Biberstein M, Parker BA. Enema-induced hyperphosphatemia. Ann J Med 1985;79:645–646. 6. Escalante CP, Weiser MA, Finkel K. Hyperphosphatemia associated with phosphorus-containing laxatives in a patient with chronic renal insufficiency. South Med J 1997;90:240–242. 7. Jorgensen LS, Center SA, Randolph JF, et al. Electrolyte abnormalities induced by hypertonic phosphate enemas in two cats. J Am Vet Med Assoc 1985;187:1367–1368. 8. Atkins CE. Hypertonic sodium phosphate intoxication. In: Kirk RW, ed. Current Veterinary Therapy IX. Philadelphia: WB Saunders, 1986:212–215. 9. Wason S, Tiller T, Cunha C. Severe hyperphosphatemia, hypocalcemia, acidosis, and shock in a 5-month-old child following the administration of an adult Fleet enema. Ann Emerg Med 1989;18:696–700. 10. Physicians Desk Reference: Montvale, New Jersey. Medical Economics, 1997. 11. Church DC. Macrominerals. In: Church DC, Pond WG, eds. Basic Animal Nutrition and Feeding. New York: John Wiley, 1988: 168–171.
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