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Veterinarian Technician April 2011 (Vol 32, No 4)

Case Report: Whole Blood Transfusion in a Duck to Correct Anemia Due to Acorn Toxicosis

by Jill Murray, RVT
    VECCS logo

    Presented at IVECCS 2010 in conjunction with Pfizer Animal Health.

    An adult male, white duck (Pekin; Anas platyrhynchos) presented as an emergency to the Zoo, Exotic and Wildlife Medicine Service of the Boren Veterinary Medical Teaching Hospital, Center for Veterinary Health Sciences, Oklahoma State University. The patient was reported to have a 7-day history of progressive inappetence, lethargy, and isolation from its flock.

    The patient was part of a mixed-species waterfowl flock residing on a public pond. The pond is routinely maintained, and the ducks are fed a commercial seed mixture three times weekly. Additionally, the ducks forage, eating a variety of plant materials and foliage as well as foods provided by visitors to the pond. The ducks have regular human contact and are reasonably social. Located in a public park, the pond is surrounded by oak trees (Quercus spp), cypress trees (Cypressus spp), grass, concrete walkways, and rocky substrate.

    The grounds crew had noticed the duck had not been feeding or socializing normally and had decreased buoyancy. The grounds crew caught the duck and brought it to the Veterinary Teaching Hospital for care.

    Initial Assessment and Triage

    On presentation, the duck was markedly weak, lethargic, and easily stressed by physical restraint. A cursory physical examination most notably revealed the crop to be markedly distended and firm. With handling, the duck regurgitated rancid seeds and plant materials. The duck was water-soaked through to its down feathers, indicating a lack of waterproofing, which surely contributed to decreased buoyancy and suspected hypothermia. The duck was emaciated (body condition score: 1/5; body weight: 1.7 kg), suggesting a chronic condition. The duck appeared to be in shock (i.e., pale, mildly cyanotic mucous membranes; a slow capillary refill time) and was estimated to be 10% dehydrated (e.g., tacky mucous membranes). An oxygen–hemoglobin saturation (SpO2) reading could not be obtained. (See BOX 1 for the normal biologic and physiologic parameters for Pekins.)

    Because the duck was severely debilitated, it was hospitalized and initially administered a subcutaneous crystalloid fluid bolus (85 mL of warmed Normosol-R [Hospira]) containing 2 mL of vitamin B complex.The patient was then placed in a warmed (85°F), oxygen-enriched incubator (40% fractional inspired oxygen) in the critical care unit (CCU) and closely monitored by visual observation.

    After a few hours, the duck appeared stronger. When a more comprehensive physical examination was performed, the duck again regurgitated rancid seeds and plant materials. In addition to the previously noted abnormalities, the only other abnormal finding was healing bilateral bumblefoot lesions. These lesions are considered to be due to abnormal wear and chronic malnutrition. Because of financial constraints and the high caseload in the CCU, the duck was moved to the exotics ward, which provided a quieter environment.

    A venous blood sample was collected to obtain a complete blood count (CBC) and plasma biochemical profile. Venous access was established via a 20-gauge, 1-inch medial–metatarsal IV catheter. Intravenous crystalloid fluid therapy (Normosol-R with 2.5% dextrose), including 5% amino acids and 2 mL of vitamin B complex, was initiated at a rate of 60 mL/kg/d, as mixed in a 1-L bag. The fluids were chosen to correct dehydration and provide partial parenteral nutrition to replace electrolytes, promote protein synthesis (to counter loss of muscle mass due to regurgitation and decreased intake), and correct suspected hypovitaminosis. Additionally, treatment with meloxicam (0.2 mg/kg SC q24h1) and enrofloxacin (10 mg/kg IM q12h1) was initiated.

    Supplemental alimentary nutrition was initiated because birds have a high metabolic rate and the patient was inappetent and markedly debilitated. A 50:50 mix of Emeraid Omnivore-Avian diet (Lafeber Company, Cornell, IL) and Oxbow Critical Care diet (Oxbow Animal Health, Murdock, NE) was prepared according to label directions and administered by oral gavage using an 18-Fr red rubber catheter. The goals of supplemental nutrition were to deliver 3% of the duck’s body weight at each of three daily feedings. The volume and frequency of nutritional support were adjusted based on a daily weight curve. Additionally, the duck was offered fresh greens, waterfowl pellets, and free-choice water.

    Pending further diagnostic testing, the patient received supportive care overnight in a room that was climate controlled at 85°F. Over the next 18 hours, the duck was observed to have marked polyuria and polydipsia (PU/PD). The duck continued to regurgitate rancid plant ingesta (including several whole acorns [Quercus spp]), the gavage formula, and large amounts of water. During this time, no fecal output was noted.

    Diagnostic Workup

    The CBC revealed marked nonregenerative anemia with a packed cell volume (PCV) of 10% (normal: 40% to 46%) and leukopenia (3.0 µg/L; normal: 10.4 to 18.0 µg/L). The plasma biochemical profile revealed hypoproteinemia (1.2 g/dL; normal: 3.6 to 6.4 g/dL), hypoalbuminemia (0.4 g/dL; normal: 1.3 to 2.6 g/dL), hypocalcemia (7.5 mg/dL; normal: 9.6 to 11.8 mg/dL), an elevated creatine phosphokinase level (15,877 IU/L; normal: 32 to 666 IU/L), a markedly elevated aspartate aminotransferase (AST) concentration (194 IU/L; normal: 4 to 46 IU/L), and an elevated uric acid level (16 mg/dL; normal: 2.0 to 7.6 mg/dL). See TABLE 1 for normal physiologic data for mallards.2

    Further workup included whole body radiography and upper gastrointestinal (GI) endoscopy with the patient under general anesthesia. The duck was premedicated with butorphanol tartrate (0.5 mg/kg IM)1 and midazolam (0.2 mg/kg IM).1 Twenty minutes later, anesthesia was induced using 5% isoflurane via face mask and a precision vaporizer (oxygen flow rate: 2 L/min). The duck was intubated with a 6-Fr, uncuffed, Murphy-eye endotracheal tube. Anesthesia was maintained using 1.5% to 2.5% isoflurane at an oxygen flow rate of 1 L/min for the duration of the procedure. An 18-gauge, 2-inch IV catheter was placed in the right jugular vein, through which 10 mL/kg/h of warmed Normosol-R with 2.5% dextrose and 2.5% amino acids was administered for the duration of the procedure. Anesthesia and postanesthetic recovery were uneventful.

    Right lateral and ventrodorsal whole body radiography revealed foodstuffs in the crop and ventriculus (FIGURE 1; FIGURE 2) . In addition, microhepatia and a generalized decreased muscle mass consistent with emaciation were noted. After radiography, upper GI endoscopy was performed using a 5.9-mm flexible video bronchoscope, revealing large quantities of rancid feedstuffs and acorns in the crop and proventriculus. Acorns (Quercus spp) were obstructing the flow of ingesta through the isthmus into the ventriculus, contributing to the patient’s regurgitation and decreased nutritional status. The contents of the crop and proventriculus were manually removed, after which the area was carefully flushed to prevent aspiration of the contents down the trachea. Multiple white plaques were found on the mucosal surfaces of the crop and proventriculus, suggesting infection with Candida spp. Candidiasis was confirmed by cytologic examination.

    Diagnosis

    Based on the patient history as well as hematologic, radiographic, and upper GI endoscopic findings, the presumptive diagnosis was oak (tannin) toxicosis with concurrent Candida albicans infection.

    Treatment

    Supportive care was continued while a blood-donor duck was sought for a whole blood transfusion to correct anemia. A female Pekin flock mate was crossmatched using a slide agglutination test and found to be an appropriate match. The donor was in good body condition (body condition score: 3/5; body weight: 2.6 kg). The donor’s PCV (30%; normal: 40% to 46%)2 and total plasma protein values (TPP; 3.0 g/dL; normal: 3.6 to 6.4 g/dL)2 were considered adequate for transfusion (FIGURE 3) . The donor was anesthetized with 5% isoflurane via face mask and precision vaporizer(oxygen flow rate: 2 L/min). Anesthesia was maintained using 1.5% isoflurane (oxygen flow rate: 1 L/min) for the duration of blood collection. The anticoagulant solutions acid citrate dextrose, citrate phosphate dextrose, and citrate phosphate dextrose adenine were not available; therefore, heparin sodium (1000 USP U/mL) was used at a ratio of 0.1 mL per 7 mL of whole blood. Because heparin sodium lacks preservatives and affects the clotting cascade, it is not an ideal anticoagulant for collection and administration of whole blood products.However, heparin sodium was considered adequate in this case because the recipient had a normal platelet count and transfusion was performed immediately.3,4

    Twenty-six milliliters of whole blood (1% of body weight) was collected from the right jugular vein of the donor via a 21-gauge, 0.75-inch butterfly catheter and syringe technique into three heparinized, 10-mL syringes. The blood was immediately placed on a rocker to reduce the risk of clotting after collection. The donor was then administered warmed Normosol-R (90 mL SC) to aid volume replacement. The donor recovered from anesthesia uneventfully and ate and drank shortly thereafter. The donor was returned to its flock the following morning.

    On day 3, without anesthesia, the anemic duck underwent blood transfusion via jugular catheter according to the hospital’s CCU aseptic protocol. During the transfusion, the duck was monitored for adverse reactions by continuous electrocardiography, periodic cardiac and respiratory auscultation, and visual observation (FIGURE 4) . The donor blood was transfused by syringe pump through an inline 50-µm pediatric filter at a rate of 2 mL/kg/h for the first 30 minutes. After no evidence of an adverse reaction, the rate was increased to 6 mL/kg/h for the following 2 hours until 26 mL was transfused. No adverse reactions were observed during or after the transfusion.

    IV fluid therapy was restarted at a rate of 60 mL/kg/d to maintain vascular volume and hydration. The bumblefoot lesions were managed conservatively by maintaining the duck on appropriate substrate and improving its nutritional status.Oral administration of enrofloxacin (5 mg/kg q12h for 10 days) and meloxicam (0.2 mg/kg q24h1 for 7 days) was continued. Oral nystatin (300,000 U/kg PO q12h1) was initiated to treat candidiasis.

    Outcome

    After the whole blood transfusion, the duck was kept in the hospital to continue supportive care and evaluate the response to treatment. Twenty-four hours after the transfusion, the duck’s PCV was 18% and TPP was 2.4 g/dL. Seventy-two hours after the transfusion, the duck remained stable with a PCV of 25% and a TPP of 3.2 g/dL, indicating a successful transfusion. Because of financial limitations and subjective clinical improvement, the CBC and plasma chemistry profile were not rechecked. The duck exhibited marked clinical improvement 96 hours after the transfusion:

    • The duck was bright, alert, active, and preening normally
    • The duck resumed eating on its own and ceased regurgitating
    • The PU/PD appeared to resolve

    The duck was weaned off supplemental nutrition by day 4 and had a steady increase in body weight, with normal fecal output, by day 6. The duck was exercised daily, including swimming to reestablish waterproofing (FIGURE 5) . Antifungal and antimicrobial therapies were continued; antiinflammatory therapy was discontinued on day 7.

    The duck showed continued daily improvement in attitude, feeding behavior, and body weight and was released to its flock at the pond 14 days after hospital admission (FIGURE 6) . At subsequent visits to the pond by hospital staff, the duck appeared normal and had resumed normal interaction with its flock. The duck could not be caught for follow-up evaluation.

    Discussion

    Tannin toxicosis resulting from ingestion of oak leaves and acorns has been reported in many species.5 Toxicosis has been most commonly identified in cattle and less commonly in sheep, goats, and horses. In North America, all of the more than 70 Quercus spp (oak) should be considered potentially toxic.6,7 Toxicity is based on the species of oak and the volume of plant ingested; any part of the oak plant can be toxic. Budding leaves and green acorns contain the highest toxin levels. Oak intoxications are most common in the spring and fall due to new bud growth and acorn development, respectively.5,6

    When ingested, the tannins and their metabolites can result in severe GI and renal dysfunction, and acorns may cause mechanical obstruction.Clinical signs of tannin toxicosis may occur several days after consumption. Delayed diagnosis can result in severe renal and hepatic impairment, which can be fatal. The only treatment for tannin toxicosis is prompt supportive care, including diuresis to clear the toxin. Diagnosis can be made with a thorough history, observation of clinical signs consistent with GI upset and PU/PD, evaluation of tannin and gallotannin levels in urine, examination of GI or rumen fluid contents and suspected plant material samples, and evaluation of necropsy and histologic findings.5,6 The presumptive diagnosis in this case was based on patient history, clinical findings of GI upset and PU/PD, and finding plant material and acorns (Quercus spp) on endoscopic examination.

    Birds may have a higher tolerance for blood loss than most mammals8 and generally respond well to supportive fluid replacement and treatment of only the underlying cause of blood loss. Avian tolerance for blood loss may be due to rapid red blood cell (RBC) regeneration, reflex vasoconstriction of the peripheral vasculature, and the ability to mobilize fluid from the extravascular space.8,9 An increase in the number of circulating immature RBCs can be detected in anemic birds within 12 hours.10,11 Blood transfusion may be indicated for birds with rapid blood loss, a PCV less than 15%, and clinical signs consistent with shock and hypoxia. A homologous (same genus and species) transfusion is preferable and was used in this duck, but heterologous (cross-species) transfusion is possible. The cell life of a homologous avian transfusion is reported to be 10 to 17 days, while that of a heterologous avian transfusion may be only 1 to 3 days.10,11 Transfusion reactions in birds appear to be rare, and pretreatment of birds with antihistamine is not routinely indicated. With repeated heterologous transfusions, crossmatching the donor and recipient is generally recommended.10,11 After transfusion, monitoring of the PCV, TPP, uric acid level, liver enzyme concentrations, and clinical response is recommended.7,9

    When blood products are not available, hetastarchmay be used to support intravascular volume.8,9 Iron dextran may be administered to markedly anemicbirdsunless sepsis or iron storage disease is suspected.8 In anemic birds, the stress of handling can increase oxygen demand. The administration of supplemental oxygen is beneficial to fully saturate the remaining RBCs with oxygen and increase the systemic arterial oxygen concentration.8

    C. albicans infection was considered to bea secondary opportunistic yeast infection in this duck.Candidaspp are normally present in low numbers in the digestive systems of birds. Generally, this yeast remains superficial; however, when the host is immunocompromised, Candidaspp can proliferate and invade deeper tissues, resulting in candidiasis. Clinical signs of GI candidiasis include regurgitation, weight loss, anorexia, diarrhea, and delayed crop emptying. Diagnosis in this duck was based on endoscopic visualization of white plaques in the digestive tract with cytology of plaque samples. Treatment of GI candidiasis requires direct contact of the fungistatic agent (by oral administration) with the organism (plaques), adequate supportive care (fluid and nutritional), and treatment of concurrent or associated conditions.12

    Conclusion

    This case appears to be unique: I am not aware of other cases of Quercus spp toxicosis in Anseriformes. A case report of fatal oak toxicosis in a double-wattled cassowary exists.13

    Pekins and Pekin hybrids are kept as pets in the United States, and owners should be cautioned about oak tannin toxicity, especially due to ingestion of oak buds in the spring and acorns in the fall.

    Limited financial resources for treating wildlife can significantly hinder diagnostic workup and treatment. Veterinary care of birds has many challenges: marked interspecies differences (wide physiologic diversity and anatomic variations), limited reference medical data, and varied nutritional and environmental requirements. In this case, as with most critically ill birds, the diagnostic workup had to be delayed until the patient could be stabilized physiologically. After stabilization, locating and obtaining blood from a suitable blood donor were challenging. This case is an excellent example of the challenges of caring for wildlife, including initial presentation, diagnostic workup, treatment, release, and followup. The successful outcome of this case was very rewarding in nonmonetary ways.

    Downloadable PDF

    1. Carpenter JW, ed. Exotic Animal Formulary. 3rd ed. St. Louis: Elsevier Saunders; 2005:134-344.

    2. International Species Information System. Accessed January 2011 at www.isis.org.

    3. Animal Blood Bank. Anticoagulants. Accessed January 2011 at www.animalbloodbank.com/education.html.

    4. Plumb DC, ed. Veterinary Drug Handbook. 6th ed. Ames, IA: Blackwell Publishing; 2008:448-451.

    5. Murray MJ, Smith BP. Disease of the alimentary tract. In: Smith BP, ed. Large Animal Internal Medicine. St. Louis: Mosby; 2002:772-773.

    6. Panter KE, Gardner ST, Lee JA, et al. Important poisonous plants of the United States. In: Gupta RC, ed. Veterinary Toxicology Basic Principles and Clinical Principles. New York: Academic Press; 2007:825-872.

    7. Burrows GE, Tyrl RJ. Fagacae. In: Toxic Plants of North America. Ames, IA: Iowa State University Press; 2001:685-700.

    8. Harrison GJ, Lightfoot TL, Flinchbaum GB. Emergency and critical care. In: Harrison GJ, Lightfoot TL, eds. Clinical Avian Medicine. Vol I. Palm Beach, FL: Spix Publishing; 2006:213-232.

    9. Dorrenstein GM. Nursing of the sick bird. In: Tully TN, Dorrenstein GM, Jones AK, eds. Handbook of Avian Medicine. 2nd ed. Philadelphia: Saunders Elsevier; 2009:101-137.

    10. Degernes LA, Crosier ML, Harrison LD, et al. Autologous, homologous, and heterologous red blood cell transfusions in cockatiels (Nymphicus hollandicus). J Avian Med Surg 1999;13(1):2-9.

    11. Degernes LA, Harrison LD, Smith DW, et al. Autologous, homologous, and heterologous red blood cell transfusions in conures of the genus Aratinga. J Avian Med Surg 1999;13(1):10-14.

    12. Dahlhausen RD. Implication of mycoses in clinical disorders. In: Harrison GJ, Lightfoot TL, ed. Clin Avian Med. Vol II. Palm Beach, FL: Spix Publishing; 2006:691-704.

    13. Kindle HA. A fatal case of oak poisoning in a double-wattled cassowary (Casuarius casuarius). Avian Dis 1988;32:849-851.

    References »

    NEXT: Final View: A "Heart" of Stone

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