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Avian obstetrics
Avian Obstetrics April Romagnano, PhD, D VM
This article reviews the following common problems encountered in avian obstetrical medicine: egg binding, dystocia, prolapsed oviduct, egg yolk peritonitis, chronic egg laying, oviduct impaction, oophoritis, salpingitis, metritis, ectopic eggs, cystic hyperplasia of the oviduct, neoplasia, and cloacal pathology. Each section defines a problem and discusses its proposed etiologies, clinical signs, and pertinent diagnostics and treatment options. Copyright9 1996by W. B. Saunders Company.
following c o m m o n problems in avian obstetrical medicine: egg binding, dystocia, prolapsed oviduct, egg yolk peritonitis, chronic egg laying, oviduct impaction, oophoritis, salpingitis, metritis, ectopic eggs, cystic hyperplasia of the oviduct, neoplasia, and cloacal pathology.
Key words: Avian obstetrics, egg binding, egg yolk peritonitis, chronic egg laying, ectopic eggs.
Egg Binding and Dystocia
ainY problems e n c o u n t e r e d in avian obstetcs n e e d immediate attention. However, most can be rectified if properly identified by using the simple techniques described in the following discussion. One necropsy study of 24 avian orders showed an 8.9% prevalence of reproductive disease. 1 Most veterinary practices fail to recognize an 8.9% incidence of reproductive disease. This suggests that education and preventative medicine may facilitate detection and therapy of avian reproductive disease. 2 Obstetrical problems are multifactorial, and prognosis varies on a case-by-case basis. The most effective way to evaluate these cases is the classic "problemioriented approach." The avian clinician must obtain a thorough general and reproductive history. Physical examination, blood work (including complete blood count [CBC] and chemistries), cloacal culture and sensitivity, and radiography are potentially indicated in obstetrical cases. However, ultrasound and endoscopy are also important diagnostic tools. The decision to proceed with diagnostics, or immediately commence emergency supportive treatment, is made on a case-by-case basis. The purpose of this r e p o r t is to review the clinical signs, diagnosis, and treatment of the
From the Avicultural Breeding and Research Cent~ Loxahatchee, FL. Address reprint requests to April Romag~ano, PhD, DI/Tvl, Staff Veterinarian, Aviculturat Breeding and Research Cente;, Loxahatchee, FL 33470. Copyright9 1996by W. B. Saunders Company. 1055-937X/96/0504-000255.00/0
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Egg binding is one of the most c o m m o n obstetric complications in birds. It is defined as the failure of an egg to pass through the oviduct at a normal rate, ie, delayed oviposition. Unfortunately, variability of egg passage rates between and within species complicates its diagnosis. 3 Typical laying intervals are greater than 24 hours but range from 24 hours in the domestic hen and passerines, 48 hours in psittacines, to 44 days in the brown kiwi. 4,5 Dystocia is defined as the mechanical obstruction of an egg in the caudal reproductive tract. 2,4 Dystocia can occur at the level of the caudal oviduct/uterus, the vagina, or the vaginal-cloacal junction. Obstruction can result in cloacal impaction a n d / o r prolapse. The cause of egg binding is multifactorial. The causes include hypocalcemia and other nutritional deficiencies, oviduct, uterus, or, vaginal muscle dysfunction, excessive egg production, large, misshapen, or soft-shelled egg(s), age of hen, obesity, oviduct tumor, oviduct infection, lack of exercise, hypertherrnia or hypothermia, and genetics. 6-9 In addition to most complications that lead to egg binding, dystocia can also result from breeding out of season, first-time layers, or hens afflicted with persistent cystic right oviduct. 10 The space-occupying effect of the egg, during dystocia, can cause various life-threatening complications. These include circulatory disorders, shock, and nerve paralysis, secondary to compression of pelvic and renal vasculature and nerves. 7 Cessation o f normal defecation and micturition can lead to severe metabolic disturbances including gastrointestinal ileus and obstructive renal disease, z,s Pressure necrosis of the three oviduc-
Seminars in Avian and Exotic Pet Medicine, Vol 5, No 4 (October), 1996:pp 180-188
Avian Obstetrics
tal layers can also occur secondary to pressure resulting in uterine or oviduct rupture. 4 The clinical signs of dystocia and egg binding vary, with bird size. Smaller species such as finches, budgerigars, cockatiels, and love birds are more commonly affected by dystocia. 4 Limited reserves, high-energy requirements, and c o m p a c t a n a t o m y warrant m o r e aggressive therapy in small versus large avian species? In general, the egg-bound or dystocia patient is usually depressed, lethargic, quiet, and tachypneic. Additionally, it has a wide n o n p e r c h i n g stance and may have unilateral or bilateral paresis/paralysis. The a b d o m e n and cloaca are usually doughy and swollen, and an egg is typically palpated in the abdomen. Tail wagging, straining, decreased defecation frequency, increased defecation volume, or dyspnea, as well as nesting behavior, also may be seen. In cases of severe dystocia, the birds feet may go "blue-white," indicating vasculature compromise and warranting immediate intervention (see ovocentesis and surgery below). Differential diagnoses for egg binding and dystocia include, but are not limited to, abdominal or oviductal tumors, abdominal herniation, or lipomas. After physical examination, patient stabilization is critical. The severity of the condition can be assessed by the level of depression, whether oviductal or cloacal tissue is prolapsed, and the location of the egg within the abdominal tract. Ideally, fluids (lactated Ringers solution [LRS] ) should be administered subcutaneously (SQ), but initially supplementation with an intravenous (IV) bolus may be n e e d e d (50 m L / k g + % dehydration, divided BID). Placement of an interosseous or IV catheter should be reserved for cases of severe dehydration. Calcium should be administered IM in all situations. Vitamin A and E / s e l e n i u m also may be helpful. The patient should be placed in a warm, humid, and steamfilled oxygenated incubator mai~ntained at approximately 90~ (32.2~ Eggs passed with this protocol could be fertile and should be incubated. 4 Depending on the condition of the patient, a CBC and chemistry panel may be warranted. Hypocalcemia, a frequent cause of egg binding, occurs secondary to low calcium diets, especially those high in fat, or aberrant calcium metabolism. 2 Hypercalcemia can be seen normally during egg laying, where blood levels can reach 30
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m g / d L or higher. 4 Eggshell calcium is normally obtained from circulating blood calcium, replenished by intestinal absorption and bone mobilization. 2,1a Much of the shell is f o r m e d at night, when food intake is nil and circulating blood calcium is decreasing, n Hence, during the early m o r n i n g hours, b o n e mobilization of calcium is highest, as is the incidence of hypocalcemic episodesJ 1 If present, prolapsed tissue should be cleaned with warm sterile saline flushes and coated with sterile lubricant. If no tissues are prolapsed and abdominal palpation does not show an egg, radiography and or ultrasound should be performed. Radiography may also show medullary bone formation, called hyperostosis or osteomyelosclerosis, which occurs u n d e r the influence of estrogen in the laying hen. 12 Physiologic hyperostosis is most commonly observed in the femur, tibiotarsus, radius, and ulna. 12 Ultrasonography is superior to radiography for the diagnosis of impacted soft-shelled eggs, ectopic soft-shelled or shell-less eggs, and salpingitis and to differentiate oviduct masses from other caudal abdominal masses. It is also a quick and easy p r o c e d u r e to p e r f o r m on the nonanesthetized avian patient but is typically limited by expense, accessibility, and size of patient. Prostaglandin E2 (PGE2) has been shown to relax the unterovaginal sphincter and increase uterine contractions. 1~ PGE2 gel (Prepidil; Pharmacia and Upjohn, Kalamazoo, MI) is recomm e n d e d topically, applied to the uterovaginal sphincter, at a dose of 0.1 mL per 100-g bird. For an overview of the clinical use of PGE2, refer to Hudelson and H u d e l s o n J 5 If the uterus is intact, free of disease or neoplasia, and the egg is not adhered to the oviduct, then the contractions produced by PGEz gel are forceful e n o u g h to expel the egg safely within 15 minutes of application. 14 The use of PGE2 gel also stimulates the endogenous release of arginine vasotocin (AVT) because it causes uterine contractions. 14 Arginine vasotocin then further enhances these contractions. 1~,14The direct release of AVT by PGE z has not been documented; further, the mechanism for AVT's release is not understood, although a neurogenic response, as in mammals, is suspected. 14 The e n d o g e n o u s release of AVT has not been reported as a problem; therefore, adverse side effects are not known at this time. PGE 2 can cause diarrhea if administered systemi-
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cally in prescribed doses, and this is its major adverse effect. This adverse side effect has not b e e n n o t e d with the topical use of PGE 2. However, a systemic overdose of PGE2 could potentially elicit excessive muscle contractions as is seen with prostaglandin" F2a (PGFz~) (see below). PGF2~ elicits generalized s m o o t h muscle contractions, and according to several authors, does not relax the uterovaginal sphincter a n d is not the prostaglandin of choice in birds. 13q~ Parenteral PGF2~ is m o r e likely to cause systemic reactions such as general smooth muscle contraction, increased b l o o d pressure, a n d b r o n c h o c o n strictions, n This combination of systemic reactions can lead to very forceful contractions that can result in uterine rupture, severe cramping, and possibly death. A different viewpoint has e m e r g e d f r o m a few e x p e r i e n c e d avian clincians regarding the usage of PGF2~ (Lutalyse-Upjohn, Kalamazoo, MI).16 Anecdotal clinical experience with this p r o d u c t has provided these clinicians with excellent clinical results, resulting in oviposition and obviating the n e e d for m o r e aggressive intervention. 16 Cases that were selected for this therapy were limited to when the egg was in "pelvic presentation. ''16 These clinicians have f o u n d this technique to provide an effective alternative to PGE2, which is reportedly h a r d to get and costly. 16 T h e a u t h o r aknowledges the experienc e of these clinicians but urges the reader to consult H u d e l s o n a~ for clarification. Oxytocin is- safer than PGF2~, as it at least targets the uterus; however, it does not relax the uterovaginal sphincter and is thus inferior to PGE2 .14,a50xytocin can elicit tail p u m p i n g , panting, and abdominal contractions that may eventually lead to oviposition. 4 However, the use of oxytocin for egg binding and dystocia is contraindicated, unless the uterovaginal sphincter is well dilated and the uterus is free of mass-occupying disease and adhesions. 14 In complicated cases and in small birds such as finches and canaries, uterine r u p t u r e can often be a sequela to oxytocin treatment. 14 If oviposition still does not occur within 24 hours after h o r m o n a l therapy or other medical t r e a t m e n t in most m e d i u m to large psittacines (or 1 h o u r in finches or o t h e r small birds) one of two nonsurgical techniques should be tried: digital pressure or ovocentesis. With the bird u n d e r isoflurane anesthesia, the cloaca is lubri-
cated and the cervix gently mechanically dilated. Persistent digital pressure is p u t on the egg in the direction of the cloaca, helping it to pass. Fingers are placed above the egg, and between it and the caudal-ventral aspect of the keel bone. T h e pressure is constant but precise, with care not to b r e a k the egg or to cause uterine or cloacal prolapse. Digital m a n i p u l a t i o n is contraindiL cated in cases of uterine constriction, torsion, rupture, or ectopic eggs. Ovocentesis is warranted, if oviposition does not occur with digital pressure. However, ovocentesis can produce sharp eggshell pieces that can cause uterine damage. In addition, retained pieces can serve as a nidus for infection. Ovocentesis, aspiration of the egg contents with a large-bore needle, is usually p e r f o r m e d transcloacally or transabdominally. Transcloacal ovocentesis is safer, especially if the egg can be visualized with a speculum through the cloaca. 4 After aspiration, the n o r m a l or hard-shell egg may n e e d to be gently collapsed. Laceration of the oviduct is possible with this technique, and care should be used when removing visible eggshell pieces. Retrograde uteral flushing with warm, sterile saline, via syringe and aided by a speculum, may aid in removing hidden eggshell pieces and reduce the incidence of metritis. 4 Soft-shell eggs, once their contents are removed, easily implode on their own, a n d may therefore pass unaided. 2 Surgical removal is warranted if the egg is lodged in the caudal oviduct or cloaca. An episiotomy should be a t t e m p t e d in these cases. 4 In cases where the egg is severely a d h e r e d to the oviduct wall, the uterus is ruptured, a soft-shelled egg is located cranial to the oviduct, or the egg is ectopic, a ventral laparotomy or possibly, a hysterectomy, is indicated. Once the egg is passed or removed, the bird needs to be followed u p closely because m a n y hens with egg binding or dystocia will lay again soon. Egg binding and dystocia can also recur with future clutches. Historically, medroxyprogesterone was used to stop ovulation after egg binding or dystocia and in cases of chronic egg laying. 2,4 This therapy is considered controversial and is not r e c o m m e n d e d by the author. However, if attempted, progesterone should only be administered after a complete clutch is laid because it may cause soft-shell eggs, mummification, peritonitis, and death. 4 In large doses 36 hours before ovulation, progesterone inhibits
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ovulation and induces follicle atresia. 4 If progesterone is administered 2 to 24 hours before ovulation, it can induce a pre-ovulatory surge of L H and premature ovulation, increasing the risk of egg yolk peritonitis and an ectopic egg. 4 O t h e r side effects ofmedroxyprogegterone include obesity, hepatic lipidosis, weight gain, lethargy, transient or persistent hyperestrogenism, polyuria, and polydipsia. O t h e r complications that occur secondary to egg binding and dystocia include cloacal, oviduct, and uteral prolapse or paralysis, egg yolk peritonitis, scarring or damage to the oviduct, ascending salpingitis or metritis, and abdominal hernias. 4,2
vents aperture while maintaining an exit for urine, urates, and feces. If the cloaca repeatedly prolapses, a cloacalpexy is warrantedJ s If treated promptly, the prognosis for prolapsed tissues is good. 7 Chronic prolapses have a p o o r prognosis for survival of the prolapsed tissue. Surgical d e b r i d e m e n t or possibly a hysterectomy may be required once the patient is stabilized, t9 If an egg is present in the tissues, it must be removed before the prolapse can be replaced. Digital pressure a n d / o r ovocentesis may be necessary in such cases.
Egg Yolk Peritonitis Prolapsed Oviduct Prolapse of the oviduct, uterus, vagina, a n d / o r cloaca can occur secondary to dystocia, normal egg laying, physiologic hyperplasia, or various disease states affecting these tissuesfi 17 Powerful abdominal contractions associated with oviposition, the size of the egg, general debilitation, and malnutrition can all contribute to oviduct prolapse. T h e uterus is most commonly prolapsed, but the vagina, and cloaca may prolapse in part. 4 The caudal oviduct may also prolapse, especially if an egg is present within the tissues. Exposed tissues are susceptible to infection and devitalization and therefore must be treated aggressively. They should be kept moist and clean with warm sterile saline flushes. Immediately before flushing, cloacal cutttire and sensitivity and a CBC and chemistry should also be obtained. Parenteral antibiotics and fluids should be administered. If no egg is present (or if it is easily passed or removed), the tissues are clean, and parenteral antibiotics have been administered, topical sterile lubricant mixed (1:1) with sterile 50% dextrose can be applied to the prolapse tissue to help decrease edema. Some authors prefer topical steroid preparations containing antibiotics or dimethyl sulfoxide gel (DMSO) to help reduce the inflammation in addition to the swelling. 4 The moistened, shrunken tissues are gently replaced with a lubricated swab. Recurrence is c o m m o n with prolapses, and re-replacement should be attempted a few times. If necessary, one stay cruciate suture can be placed laterally on either side of the vent to help prevent reprolapse and allow the tissues to regress in size naturally. This stay suture technique reduces the
Septic egg yolk peritonitis is a term used to describe a highly fatal condition associated with the presence of infection and egg yolk material in the coelomic cavity. 1,2,4Nonseptic yolk peritonitis has a better prognosis because the yolk itself only causes a mild histiocytic response and is gradually reabsorbed if no infection is present. A group of syndromes may contribute to egg yolk peritonitis and include ectopic ovulation secondary to reverse peristalsis, salpingitis, metritis, neoplasia, cystic hyperplasia, r u p t u r e d oviducts, and stress or physical restraint of the egg-laying hen. 4 Acute signs of egg yolk peritonitis include decreased or ceased egg production, depression, anorexia, mild weight loss, a history of broodiness, or recent egg laying. 2,4,2~ Diagnosis and immediate treatment improves prognosis of such cases. Abdominal swelling and ascites are comm o n chronic clinical signs, especially in smaller psittacines. Respiratory distress and sudden death may be associated with these cases. Ascites is rarely seen in macaws. Acute egg yolk peritonitis causes a severe inflammatory response, paralleled by that typically seen with chlamydia, aspergillosis, and osteomyelitis infections, where WBC counts may be greater then 30,000 WBC/txL. Radiography, abdominocentesis, endoscopy, and laparotomy are helpful diagnostic aids. Egg yolk peritonitis is most frequently described in cockatiels, budgerigars, lovebirds, ducks, and macaws, especially scarlet macaws. 19,z~O t h e r syndromes associated with egg yolk peritonitis include egg-related pancreatitis, which may lead to temporary diabetes mellitus, and yolk emboli, which can result in a strokelike syndrome, especially in cockatiels.
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Treatment fo r egg yolk peritonitis depends on the severity of the clinical signs. 2 Traditional medical m a n a g e m e n t of chronic cases includes long-term parenteral antibiotics based on culture and sensitivity and supportive care as needed, including abdominocentesis to reduce abdominal pressure and relieve dyspnea. 2,4 The etiologic agent of egg-related peritonitis is often coliforms, especially Escherichia coli. Yersinia pseudotuberculosis and Staphylococcus spp have been rep o r t e d in association with egg-related peritonitis. Anaerobes and chlamydia have also b e e n implicated. Endoscopy should be p e r f o r m e d in the stabilized patient to assess the severity of the internal pathology associated with egg yolk peritonitis, z Care must be used to minimize ascites before endoscopy or surgery and to position the patient on an incline with the head elevated. If this is not p e r f o r m e d , the bird could drown because the integrity of the airsacs, compartmentalizing the fluid away from the lungs, is the only protection in avian species because they lack a diaphragm. If an excessive a m o u n t of yolk, an inspissated egg, or adhesions exist, then surgery, consisting of a laparotomy with abdominal flushing, is indicated in the stabilized patient. 2,4 Surgical treatment of scarlet macaws has been successful. a9 Prognosis is d e p e n d e n t on p r o m p t detection and early treatment. 2,4 Traditionally it has been believed that most cases resolve with medical therapy alone when detected early in the acute stage. However, chronic egg yolk peritonitis remains the most c o m m o n fatal obstetrical condition in avian species. 1,2,4
Chronic Egg Laying Chronic or excessive egg laying occurs when a hen has repeat clutches, regardless of the presence of a natural mate or the p r o p e r breeding season, or when she lays larger-then-normal clutch sizes. 2,4 T h i s p h e n o m e n o n occurs commonly in cockatiels, budgerigars, and lovebirds, and infrequently occurs in hand-raised psittacine hens that are imprinted on humans. 2,4 The etiology of excessive or chronic egg laying is multifactorial. Malnutrition, genetics, sexual stimulation, photoperiod, and the presence of eggs in their nest, for example, all directly or indirectly affect the bird's h o r m o n a l balance, and ultimately, egg laying. Excessive or chronic egg laying leads to calcium deficiency,
and eventually egg binding, osteoporosis, and severe malnutrition. 2 Malnutrition resulting directly from a p o o r diet, coupled with the calcium depletion of egg laying, exacerbates this phenomenon. As previously mentioned, genetics is known to be responsible for the occurrence of this syndrome in cockatiels, budgerigars, and lovebirds. 2 Sexual stimulation induced by toys, nest boxes, h u m a n beings, inappropriate mates, or natural mates should be eliminated. Decreasing the p h o t o p e r i o d to 8 to 10 hours of light per day interrupts the h o r m o n a l balance, ceasing egg production. The eggs of an excessive or chronic egg layer should be left in the nest or replaced with artificial ones because an empty nest stimulates the h e n to lay again, exacerbating the problem.Z, 4 Clinical signs attributable to end-stage chronic egg laying, in addition to excess egg production, include weight loss and dehydration secondary to chronic regurgitation, feather loss and dermatitis around the vent secondary to masturbation, and abnormal egg production, oviduct inertia, muscular weakness, and pathological fractures secondary to chronic calcium depletion. 2,4Unfortunately, these late signs are typically the first ones noted. Acute or early clinical signs include repetitive or increased frequency of egg laying, increased numbers of eggs layed, and excessive broodiness. These signs are particularly noticeable in detei~minant layers who will normally only lay a set n u m b e r of eggs per clutch regardless of removal or destruction, ie, budgerigars. The majority of parrots are believed to be indeterminant layers who will continue to lay after egg removal or destruction until they recognize the correct n u m b e r of eggs in their clutch. Treatment of chronic or excessive egg laying includes addressing malnutrition, beginning medical/pharmacological treatment, and potentially salpingiohysterectomy. 2 Nutritional a n d / o r vitamin supplementation should be addressed in all cases. Pharmacological medical m a n a g e m e n t of chronic egg layers is controversial and varied. Medroxyprogesterone injections or implants have historically been used in cases of chronic egg laying to interrupt the laying/ovulatory cycle. However, this practice is controversial owing to various side effects including obesity, hepatic lipidosis, weight gain, lethargy, polyuria, and polydipsia. 4,19,22
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As previously mentioned, progesterone should only be administered after a complete clutch is laid. In the case of the chronic egg-laying cockatiel with ascites and nonseptic egg yolk peritonitis, some authors have advocated the use of IM m e d r o x y p r o g e s t e r o n e acetate and dexamethasone. s The side effects of m e d r o x y p r o g e s t e r o n e acetate are numerous, and although they do have a place in avian medicine, they should be used with caution. D e x a m e t h a s o n e should also be used with caution; side effects include i m m u nosuppression, elevated liver enzymes, polyuria, polydipsia, and diarrhea. 2a Oral a n d parenteral testosterone have also b e e n administered in an a t t e m p t to i n t e r r u p t the ovulatory cycle, with varied success. 4 Long-acting leuprolide acetate (Lupron; TAP Pharmaceuticals, Deerfield, IL), a superactive gonadotropin-releasing h o r m o n e (GNRH) has b e e n safely used to reversibly prevent egg laying in cockatiels. 24,25 A p o t e n t G N R H agonist, Lupron, causes pituitary shut down when sustained at high levels over time. Cockatiels injected every 18 days with 100 b~g/kg cease chronic egg laying. 25 Budgerigars n e e d to be injected every 12-14 days with the same dose to achieve the same effect. 25 It has b e e n suggested by some authors that the L H activity of h u m a n chorionic gonadotrophin (HCG) administered at the appropriate stage of follicular d e v e l o p m e n t may cause follicular atresia and therefore may be used as a means to control ovulation. 26 Doses of 500 to 1000 I U / k g IM are generally effective but may n e e d to be r e p e a t e d every 3 to 6 weeks. 26 Ultimately, only a salpingiohysterectomy will stop a chronic egg layer. This p r o c e d u r e is generally considered safe in most m e d i u m - to large-sized psittacines and is also possible in cockatiels, budgies, and lovebirds for skilled surgeons. If left untreated, chronic or excessive egg laying can lead to egg binding, osteoporosis, and severe' malnutrition; thus, preventative medicine and client e d u c a t i o n is very i m p o r t a n t in the t r e a t m e n t of this condition. 2
Oviduct Impaction An impacted oviduct is usually distended and contains m u c h caseous material and misshapen, partially formed, or r u p t u r e d eggs. Oviduct impactions are often associated with salpingitis but
can also occur after metritis, egg binding, or tumors. 4 Cockatiels, canaries, and budgerigars are c o m m o n l y affected, but oviduct impaction has also b e e n r e p o r t e d in African Grey Parr o t s . 17'27"29 Salpingitis and oviduct impaction are m o r e c o m m o n l y associated with older birds. 1 Causes of oviduct impactions include excess mucin or albumin secretion secondary to cystic hyperplasia or inspissated egg material in the m a g n u m . 4 Eggs can impact in the distal oviduct if they are soft or abnormally shaped or even if they are normal. 4 Clinical signs may be mild or could include cessation of egg production, debilitation, constipation, diarrhea, a pasted vent, diffuse or unilateral (usually left side) abdominal swelling, and anorexia. 4 F u r t h e r m o r e , the bird may not be able to walk or fly. Radiology and ultrasound are useful diagnostic aids. However, endoscopy, laparotomy, or necropsy are usually n e e d e d for a definitive diagnosis. T r e a t m e n t includes cloacal/oviduct culture a n d sensitivity, long-term parenteral antibiotics, and, in most cases, salpingiotomy to clean out a n d debride the oviduct. Possibly, a salpingiohysterectomy may be needed, as the integrity of the uterine wall may not allow for healing after salpingiotomy. 4
Oophoritis Oophoritis, or an infection Of the ovary, is a reflection of the patient's health status and is frequently associated with systemic bacterial disease and sepsis, a~ T h e condition is serious and results in peritonitis and potentially death if not identified early and treated. Clinical signs include depression, anorexia, chronic wasting, and sudden death. 3~ Diagnostics include t h o r o u g h endoscopic evaluation, taking care to identify wrinkled, black, enlarged, firm, hemorrhagic, and attached or free coagulated ovum. 4 T h e r a p y includes supportive care and parenteral antibiotics as indicated by cloacal culture and sensitivity. 4
Salpingitis and Metritis Salpingitis occurs most c o m m o n l y in adult hens but is also seen in younger birds. T h e infection may be descending, secondary to air sacculitis, or p n e u m o n i a , or ascending, f r o m the distal uterus, vagina, or cloaca. Salpingitis has
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been associated with oviductal impaction, especially in passerines as well as with foreign bodies or excessive abdominal faL 2,8,31,32 E. coli is the most c o m m o n isolate, but Streptococcus spp, Mycoplasma gallisepticum, Salmonella spp, and Pasteurella multocida have b e e n implicated from various species. 4,33 Metritis is localized within the uterine portion of the oviduct and is typically a sequela to dystocia, egg binding, or chronic oviduct impaction. 4 One clinical sign associated with metritis is abnormal thickness, shape, and size o f eggs. Infections can occur in embryos or neonates secondary to metritis. Metritis may also cause egg binding, uterine rupture, peritonitis, and septicemia. 4 E coli is commonly isolated, but other coliforms have also been implicated. Severely affected birds may have an enlarged a b d o m e n and a palpable turgid uterus. 4 Radiographs typically show p o o r coelomic cavity detail. However, ultrasound is an excellent tool for evaluating oviduct size, shape, and contents in most medium- to large-sized psittacines. Clinical signs for both salpingitis and metritis may include weight loss, abdominal enlargement, and depression. 4 A discharge from the cloaca may also occur, and it is important to do cultures and sensitivities. CBC usually shows a severe leucocytosis. Treatment includes supportive care, long-term antibiotics, and retrograde direct or indirect oviduct flushing. Nonresponsive cases may n e e d surgery. Necrotic tissue should be removed via laparotomy and opening of uterus, and exudates and egg material should be removed by n o r m o g r a d e flushing or irrigation.
Ectopic Eggs Ectopic eggs result from the failure of the infundibulum to enguIf an ovum, a r u p t u r e d oviduct, or a discontinuous o v i d u c t . 4 Causes of infundibulum failure include exuberant reverse peristalsis, oviduct fat, trauma, or disease. 4 Physical restraint may also cause ectopic ovulation, therefore mating hens in season should be examined only when absolutely necessary. 3~ Ectopic ovulation occurs frequently in birds, and reportedly 28.6% in one study of nine avian orders. 1 Oviduct rupture occurs secondary to multiple pathologic conditions affecting the oviduct including large oddly shaped eggs, severe impac-
tion, egg binding, cystic hyperplasia, salpingitis, or neoplasia. Diagnosis is based on clinical signs, radiography, and ultrasound. Affected hens are depressed, lose weight, have a penguinlike stance, and have ascites. Removal or repair of damaged oviductal tissue is imperative. 4 The patient should be stabilized with rest, fluids, calcium, and broad spectrum antibiotics, pending cloacal culture and sensitivity. If the oviduct is repairable, it is flushed with warm saline and dilute chlorehexidine and surgically debrided as necessary. 4 The coelomic cavity is flushed with warm saline during oviductal surgery. Hence, eggs, caseated material, a n d / o r egg parts are removed.
Cystic Hyperplasia of the Oviduct Cystic hyperplasia of the oviduct has been reported in psittacines, especially budgerigars25 The oviduct is typically dilated with white or brown mucoid fluid and white to beige creamy masses. Clinical signs include ascites, abdominal distention, and respiratory distress. Diagnosis is based on abdominal palpation, clinical signs, radiology, and ultrasound. Treatment entails supportive care, antibiotics, based on cloacal culture and sensitivity, and salpingiohysterectomy is curative, as the problem tends to recur.
Congenital Defects Rudimentary right oviducts when present can develop cysts of significant size that could contribute to egg binding. This condition has been identified in the budgerigar. 1 Treatment is cyst removal when possible. Discontinuous or atretic oviducts have been identified in domestic fowl and can lead to ectopic eggs a n d / o r egg yolk peritonitis. 4
Neoplasia Ovarian neoplasia is more c o m m o n than oviduct neoplasia in psittacinesY Both have been described with increased frequency in the budgerigar. 27 Cloacal carcinomas are infrequent, characterized by dysplastic pleomorphic cells with bizarre mitosis. These tumors are transmurally invasive and hence may be associated with sclerosing fibroplasia, a4 Ovarian tumors can enlarge to one third the bird's body weight causing
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massive o r g a n d i s p l a c e m e n t . H e r n i a t i o n , ascites, a n d cysts a r e f r e q u e n t s e q u e l a e to n e o p l a s i a o f t h e o v a r y a n d oviduct. T h e m o s t s i g n i f i c a n t clinical sign s e c o n d a r y to a b d o m i n a l e n l a r g e m e n t is d y s p n e a , b u t c e r e c o l o r c h a n g e s a r e also o b s e r v e d in t h e b u d g e r i g a r , as is u n i l a t e r a l o r b i l a t e r a l paresis o r paralysis. D i a g n o s i s i n c l u d e s p a l p a t i o n , r a d i o g r a p h y , a n d u l t r a s o u n d b u t is b e s t b a s e d o n l a p a r o t o m y , biopsy, with o r w i t h o u t mass excision, a n d h i s t o p a t h o l o g y . 4 C o m m o n l y reported ovarian tumors include adenocarcinomas, a d e n o m a s , g r a n u l o s a cell t u m o r s , l i p o m a s , f i b r o s a r c o m a s , a n d c a r c i n o m a t o s i s . O v i d u c t a l tumors include adenomatous hyperplasia, adenocarcinomas, adenomas, and carcinomatosis. 4
Cloacal Pathology Cloacitis, cloacal strictures, cloacaliths, c h r o n i c cloacal p r o l a p s e s , cloacat p a p i l l o m a s , c l o a c a l h y p e r p l a s i a o r a d e n o m a t o u s polyps, a n d excessive c l o a c a l fat, s u r r o u n d i n g f e a t h e r s , o r p e n d u lous a b d o m i n a l l i p o m a s c a n all physically interfere with egg-laying a n d c o p u l a t i o n . T M E a c h c o n d i t i o n m u s t b e a d d r e s s e d medically, with a full w o r k - u p , a n d , w h e n necessary, c o r r e c t i v e s u r g e r y s h o u l d b e p e r f o r m e d . Cloacaliths, strictures, p r o l a p s e s , a n d p a p i l l o m a s o f t e n r e q u i r e surgical i n t e r v e n t i o n . C l o a c a l i t h r e m o v a l is o f t e n rewarding, whereas strictures are often complex a n d difficult to resolve. C l o a c a l p a p i l l o m a s p r e sent a unique and potentially infectious problem. A l t h o u g h o f u n k n o w n o r i g i n , a virus is s u s p e c t e d , a n d i s o l a t i o n o f i n f e c t e d i n d i v i d u a l s is r e c o m m e n d e d . 4 However, eggs o f p a p i l l o m a positive Blue a n d G o l d Macaws, p u l l e d at day o n e a n d artificially i n c u b a t e d , have b e e n s h o w n to p r o d u c e h e a l t h y chicks in o n e s t u d y o v e r a period of 7 yearsY
Conclusion M a n y p r o b l e m s e n c o u n t e r e d in avian obstetrics n e e d i m m e d i a t e a t t e n t i o n , h e n c e p r o p e r i d e n t i f i c a t i o n a n d t r e a t m e n t is i m p e r a t i v e . T h e classic " p r o b l e m - o r i e n t e d a p p r o a c h , " c o u p l e d with k n o w l e d g e o f t h e c o m m o n o b s t e t r i c a l diseases a n d p r e v e n t a t i v e m e d i c i n e skills, s h o u l d facilitate early detection and appropriate therapy. 2 O f t h e c o m m o n p r o b l e m s in avian o b s t e t r i c a l m e d i c i n e d i s c u s s e d previously, e g g
binding, egg yolk peritonitis, and chronic egg laying a r e m o s t f r e q u e n t l y e n c o u n t e r e d . Because obstetrical problems are multifactorial a n d p r o g n o s i s varies b e t w e e n individuals, t h e d e c i s i o n to p r o c e e d with d i a g n o s t i c s o r i m m e d i ately c o m m e n c e e m e r g e n c y s u p p o r t i v e treatm e n t is case b a s e d . H e n c e , n o t o n l y is p r o p e r d i s e a s e d e t e c t i o n i m p o r t a n t , b u t t h e avian clinic i a n m u s t b e sensitive to e a c h p a t i e n t ' s indiv i d u a l level o f debility.
References 1. Keymer IF: Disorders of the avian female reproductive system. Avian Pathol 9:405-419, 1980 2. Speer B: Clinical reproductive avian medicine, in Foundations in Avian Medicine. Proceedings of the Association of Avian Veterinarians. Philadelphia, PA, 1995, pp 23-33 3. Astheimer LB: Long laying intervals: A possible mechanism and its applications. Auk 102: 401-409, 1985 4. Joyner KL: Theriogenology, in Ritchie BW, Harrison GJ, Harrison LR (eds): Avian Medicine: Principles and Application. Lake Worth, FL, Wingers, 1994, pp 748-804 5. King SA, McLelland J: Female reproductive system, in King SA, McLelland J (eds): Birds: Their Structure and Function. Philadelphia, PA, Bailliere Tindall, 1984, pp 145-174
6. Harrison GJ: Reproductive medicine, in Harrison GJ , Harrison LR (eds) : Avian Medicine and Surgery. Philadelphia. PA, Saunders, 1986, pp 620-633 7. HashlotJ: Disease of the female reproductive organs of pet birds. J Small Anita Pract 32:313-320, 1966 8. Rosskopf WJ, Woerpel RW: Egg binding in caged and aviary birds. Mod Vet Pract 65: 437440, 1985 9. Smith RE: Hysterectomy to relieve reproductive disorders in birds. Avian Exotic Pract 2:40-43, 1985 10. Hochleithner M, Lechner C: Egg binding in a budgerigar caused by a cyst of the right oviduct. Assoc Avian Vet Today 2:136-138, 1988 11. Johnson AL: Reproduction in the female, in Sturkie PD (ed): Avian Physiology (ed 4). New York, SpringerVerlag, 1986, pp 403-431 12. Quessenberry KE, Hillyer EV: Supportive care and emergency therapy, in Ritchie BW, Harrison GJ, Harrison LR (eds) : Avian Medicine: Principles and Application. Lake Worth, FL, Wingers, 1994, pp 382-416 13. Hudelson S, Hudelson P: Egg Binding, hormonal control, and therapeutic considerations. Compend Contin Educ 15: 427-432, 1993 14. Hudelson S: Personal communication, February 1996 15. Hudelson KS, Hudelson P: A brief review of the female avian reproductive cycle with special emphasis on the role of prostaglandins and clinical applications. J Avian Med 10:67-74, 1996 16. Fudge AM, Van Sant F, Zantop D: Personal communication,July 1996 17. BeachJE: Diseases of budgerigars and other cage birds: A summary of postmortem findings. Vet Rec 74:63-68, 1962 18. Rosskopf WJ, Woerpel RW: Cloacal conditions in pet birds, with a cloacalpexy update. Proceedings of the
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25. 26. 27.
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Association of Avian Veterinarians. Seattle,WA, 1989, pp 213-231 Rosskop'fWJ, Woerpel RW: Pet avian obstetrics. Proceedings of the First International Conference of Zoological and Avian Medicine, Oahu, HI, 1987, pp 213-231 Speer BL : Non-infectious disease, in AbramsonJ, Speer BL, ThompsonJB (eds): The Large Macaws: Their Care, Breeding and Conservation. Fort Bragg, CA, Raintree Publications, 1995, pp 316-333 Rosskopf WJ, Woerpel RW: Psittacine conditions and syndromes. Proceedings of the Association of Avian Veterinarians. Phoenix, AZ, 1990, pp 432-459 Harrison GJ: Progesterone implants in cases of chronic egg laying in cockatiels. Proceedings of the Association of Avian Veterinarians. Seattle, WA, 1989, pp 6-10 Ritchie BW, Harrison, GJ: Formulary, in Ritchie BW, Harrison GJ , Harrison LR (eds): Avian Medicine: Principles and Application. Lake Worth, FL, Wingers, 1994, pp 457-478 Millam JR, Finney H: Leuprolide acetate can reversibly prevent egg laying in cockatiels. Proceedings of the Association of Avian Veterinarians, Nashville TN, 1989, pp 46 Orosz S: Personal communication, February 1996 Lighffoot T: Personal communication, February 1996 Blackmore DK, CooperJE: Diseases of the reproductive system, in Petrak ML (ed): Diseases of Cage and Aviary Birds (ed 2). Philadelphia, PA, 1982, pp 458-467
28. Degernes L: Chronic oviduct obstruction and salpingitis in an African grey parrot. Proceedings of the Association of Avian Veterinarians. New Orleans, LA, 1992, pp 156-157 29. Degernes L: Abdominal mass due to chronic salpingitis in an African grey parrot (Psittacus erithacus). Vet Pad US 34: 24-28, 1993 30. Peckham MC: Reproductive disorders, in Biester HE, Peckham MC (eds): Diseases of Poultry(ed 5). Ames, IA, Iowa State University Press, 1965, pp 1201-1205 31. Keymer IF: The diagnosis and treatment of some diseases of seed-eating passerine birds. Mod Vet Pract 40:30-34, 1959 32. Reece RL: Reproductive diseases, in Burr E (ed): Companion Bird Medicine. Ames, IA, Iowa State University Press, 1987, pp 89-100 33. Gross WB: Colibacillosis, in Calnek BW, Barnes HJ, Beard CW, et al (eds): Diseases of Poultry (ed 9). Ames, IA, Iowa State University Press, 1991, pp 138-144 34. Latimer KS: Oncology, in Ritchie BW, Harrison GJ , Harrison LR (eds): Avian Medicine: Principles and Application. Lake Worth, FL, Wingers, 1994, pp 640-672 35. Bond M: Utilizing papilloma infected blue and gold macaws (/Era araruna) in a breeding collection. Proceedings of the Association of Avian Veterinarians. Philadelphia, PA, 1995, pp 469472
This article reviews the following common problems encountered in avian obstetrical medicine: egg binding, dystocia, prolapsed oviduct, egg yolk peritonitis, chronic egg laying, oviduct impaction, oophoritis, salpingitis, metritis, ectopic eggs, cystic hyperplasia of the oviduct, neoplasia, and cloacal pathology. Each section defines a problem and discusses its proposed etiologies, clinical signs, and pertinent diagnostics and treatment options. Copyright9 1996by W. B. Saunders Company.
following c o m m o n problems in avian obstetrical medicine: egg binding, dystocia, prolapsed oviduct, egg yolk peritonitis, chronic egg laying, oviduct impaction, oophoritis, salpingitis, metritis, ectopic eggs, cystic hyperplasia of the oviduct, neoplasia, and cloacal pathology.
Key words: Avian obstetrics, egg binding, egg yolk peritonitis, chronic egg laying, ectopic eggs.
Egg Binding and Dystocia
ainY problems e n c o u n t e r e d in avian obstetcs n e e d immediate attention. However, most can be rectified if properly identified by using the simple techniques described in the following discussion. One necropsy study of 24 avian orders showed an 8.9% prevalence of reproductive disease. 1 Most veterinary practices fail to recognize an 8.9% incidence of reproductive disease. This suggests that education and preventative medicine may facilitate detection and therapy of avian reproductive disease. 2 Obstetrical problems are multifactorial, and prognosis varies on a case-by-case basis. The most effective way to evaluate these cases is the classic "problemioriented approach." The avian clinician must obtain a thorough general and reproductive history. Physical examination, blood work (including complete blood count [CBC] and chemistries), cloacal culture and sensitivity, and radiography are potentially indicated in obstetrical cases. However, ultrasound and endoscopy are also important diagnostic tools. The decision to proceed with diagnostics, or immediately commence emergency supportive treatment, is made on a case-by-case basis. The purpose of this r e p o r t is to review the clinical signs, diagnosis, and treatment of the
From the Avicultural Breeding and Research Cent~ Loxahatchee, FL. Address reprint requests to April Romag~ano, PhD, DI/Tvl, Staff Veterinarian, Aviculturat Breeding and Research Cente;, Loxahatchee, FL 33470. Copyright9 1996by W. B. Saunders Company. 1055-937X/96/0504-000255.00/0
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Egg binding is one of the most c o m m o n obstetric complications in birds. It is defined as the failure of an egg to pass through the oviduct at a normal rate, ie, delayed oviposition. Unfortunately, variability of egg passage rates between and within species complicates its diagnosis. 3 Typical laying intervals are greater than 24 hours but range from 24 hours in the domestic hen and passerines, 48 hours in psittacines, to 44 days in the brown kiwi. 4,5 Dystocia is defined as the mechanical obstruction of an egg in the caudal reproductive tract. 2,4 Dystocia can occur at the level of the caudal oviduct/uterus, the vagina, or the vaginal-cloacal junction. Obstruction can result in cloacal impaction a n d / o r prolapse. The cause of egg binding is multifactorial. The causes include hypocalcemia and other nutritional deficiencies, oviduct, uterus, or, vaginal muscle dysfunction, excessive egg production, large, misshapen, or soft-shelled egg(s), age of hen, obesity, oviduct tumor, oviduct infection, lack of exercise, hypertherrnia or hypothermia, and genetics. 6-9 In addition to most complications that lead to egg binding, dystocia can also result from breeding out of season, first-time layers, or hens afflicted with persistent cystic right oviduct. 10 The space-occupying effect of the egg, during dystocia, can cause various life-threatening complications. These include circulatory disorders, shock, and nerve paralysis, secondary to compression of pelvic and renal vasculature and nerves. 7 Cessation o f normal defecation and micturition can lead to severe metabolic disturbances including gastrointestinal ileus and obstructive renal disease, z,s Pressure necrosis of the three oviduc-
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tal layers can also occur secondary to pressure resulting in uterine or oviduct rupture. 4 The clinical signs of dystocia and egg binding vary, with bird size. Smaller species such as finches, budgerigars, cockatiels, and love birds are more commonly affected by dystocia. 4 Limited reserves, high-energy requirements, and c o m p a c t a n a t o m y warrant m o r e aggressive therapy in small versus large avian species? In general, the egg-bound or dystocia patient is usually depressed, lethargic, quiet, and tachypneic. Additionally, it has a wide n o n p e r c h i n g stance and may have unilateral or bilateral paresis/paralysis. The a b d o m e n and cloaca are usually doughy and swollen, and an egg is typically palpated in the abdomen. Tail wagging, straining, decreased defecation frequency, increased defecation volume, or dyspnea, as well as nesting behavior, also may be seen. In cases of severe dystocia, the birds feet may go "blue-white," indicating vasculature compromise and warranting immediate intervention (see ovocentesis and surgery below). Differential diagnoses for egg binding and dystocia include, but are not limited to, abdominal or oviductal tumors, abdominal herniation, or lipomas. After physical examination, patient stabilization is critical. The severity of the condition can be assessed by the level of depression, whether oviductal or cloacal tissue is prolapsed, and the location of the egg within the abdominal tract. Ideally, fluids (lactated Ringers solution [LRS] ) should be administered subcutaneously (SQ), but initially supplementation with an intravenous (IV) bolus may be n e e d e d (50 m L / k g + % dehydration, divided BID). Placement of an interosseous or IV catheter should be reserved for cases of severe dehydration. Calcium should be administered IM in all situations. Vitamin A and E / s e l e n i u m also may be helpful. The patient should be placed in a warm, humid, and steamfilled oxygenated incubator mai~ntained at approximately 90~ (32.2~ Eggs passed with this protocol could be fertile and should be incubated. 4 Depending on the condition of the patient, a CBC and chemistry panel may be warranted. Hypocalcemia, a frequent cause of egg binding, occurs secondary to low calcium diets, especially those high in fat, or aberrant calcium metabolism. 2 Hypercalcemia can be seen normally during egg laying, where blood levels can reach 30
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m g / d L or higher. 4 Eggshell calcium is normally obtained from circulating blood calcium, replenished by intestinal absorption and bone mobilization. 2,1a Much of the shell is f o r m e d at night, when food intake is nil and circulating blood calcium is decreasing, n Hence, during the early m o r n i n g hours, b o n e mobilization of calcium is highest, as is the incidence of hypocalcemic episodesJ 1 If present, prolapsed tissue should be cleaned with warm sterile saline flushes and coated with sterile lubricant. If no tissues are prolapsed and abdominal palpation does not show an egg, radiography and or ultrasound should be performed. Radiography may also show medullary bone formation, called hyperostosis or osteomyelosclerosis, which occurs u n d e r the influence of estrogen in the laying hen. 12 Physiologic hyperostosis is most commonly observed in the femur, tibiotarsus, radius, and ulna. 12 Ultrasonography is superior to radiography for the diagnosis of impacted soft-shelled eggs, ectopic soft-shelled or shell-less eggs, and salpingitis and to differentiate oviduct masses from other caudal abdominal masses. It is also a quick and easy p r o c e d u r e to p e r f o r m on the nonanesthetized avian patient but is typically limited by expense, accessibility, and size of patient. Prostaglandin E2 (PGE2) has been shown to relax the unterovaginal sphincter and increase uterine contractions. 1~ PGE2 gel (Prepidil; Pharmacia and Upjohn, Kalamazoo, MI) is recomm e n d e d topically, applied to the uterovaginal sphincter, at a dose of 0.1 mL per 100-g bird. For an overview of the clinical use of PGE2, refer to Hudelson and H u d e l s o n J 5 If the uterus is intact, free of disease or neoplasia, and the egg is not adhered to the oviduct, then the contractions produced by PGEz gel are forceful e n o u g h to expel the egg safely within 15 minutes of application. 14 The use of PGE2 gel also stimulates the endogenous release of arginine vasotocin (AVT) because it causes uterine contractions. 14 Arginine vasotocin then further enhances these contractions. 1~,14The direct release of AVT by PGE z has not been documented; further, the mechanism for AVT's release is not understood, although a neurogenic response, as in mammals, is suspected. 14 The e n d o g e n o u s release of AVT has not been reported as a problem; therefore, adverse side effects are not known at this time. PGE 2 can cause diarrhea if administered systemi-
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cally in prescribed doses, and this is its major adverse effect. This adverse side effect has not b e e n n o t e d with the topical use of PGE 2. However, a systemic overdose of PGE2 could potentially elicit excessive muscle contractions as is seen with prostaglandin" F2a (PGFz~) (see below). PGF2~ elicits generalized s m o o t h muscle contractions, and according to several authors, does not relax the uterovaginal sphincter a n d is not the prostaglandin of choice in birds. 13q~ Parenteral PGF2~ is m o r e likely to cause systemic reactions such as general smooth muscle contraction, increased b l o o d pressure, a n d b r o n c h o c o n strictions, n This combination of systemic reactions can lead to very forceful contractions that can result in uterine rupture, severe cramping, and possibly death. A different viewpoint has e m e r g e d f r o m a few e x p e r i e n c e d avian clincians regarding the usage of PGF2~ (Lutalyse-Upjohn, Kalamazoo, MI).16 Anecdotal clinical experience with this p r o d u c t has provided these clinicians with excellent clinical results, resulting in oviposition and obviating the n e e d for m o r e aggressive intervention. 16 Cases that were selected for this therapy were limited to when the egg was in "pelvic presentation. ''16 These clinicians have f o u n d this technique to provide an effective alternative to PGE2, which is reportedly h a r d to get and costly. 16 T h e a u t h o r aknowledges the experienc e of these clinicians but urges the reader to consult H u d e l s o n a~ for clarification. Oxytocin is- safer than PGF2~, as it at least targets the uterus; however, it does not relax the uterovaginal sphincter and is thus inferior to PGE2 .14,a50xytocin can elicit tail p u m p i n g , panting, and abdominal contractions that may eventually lead to oviposition. 4 However, the use of oxytocin for egg binding and dystocia is contraindicated, unless the uterovaginal sphincter is well dilated and the uterus is free of mass-occupying disease and adhesions. 14 In complicated cases and in small birds such as finches and canaries, uterine r u p t u r e can often be a sequela to oxytocin treatment. 14 If oviposition still does not occur within 24 hours after h o r m o n a l therapy or other medical t r e a t m e n t in most m e d i u m to large psittacines (or 1 h o u r in finches or o t h e r small birds) one of two nonsurgical techniques should be tried: digital pressure or ovocentesis. With the bird u n d e r isoflurane anesthesia, the cloaca is lubri-
cated and the cervix gently mechanically dilated. Persistent digital pressure is p u t on the egg in the direction of the cloaca, helping it to pass. Fingers are placed above the egg, and between it and the caudal-ventral aspect of the keel bone. T h e pressure is constant but precise, with care not to b r e a k the egg or to cause uterine or cloacal prolapse. Digital m a n i p u l a t i o n is contraindiL cated in cases of uterine constriction, torsion, rupture, or ectopic eggs. Ovocentesis is warranted, if oviposition does not occur with digital pressure. However, ovocentesis can produce sharp eggshell pieces that can cause uterine damage. In addition, retained pieces can serve as a nidus for infection. Ovocentesis, aspiration of the egg contents with a large-bore needle, is usually p e r f o r m e d transcloacally or transabdominally. Transcloacal ovocentesis is safer, especially if the egg can be visualized with a speculum through the cloaca. 4 After aspiration, the n o r m a l or hard-shell egg may n e e d to be gently collapsed. Laceration of the oviduct is possible with this technique, and care should be used when removing visible eggshell pieces. Retrograde uteral flushing with warm, sterile saline, via syringe and aided by a speculum, may aid in removing hidden eggshell pieces and reduce the incidence of metritis. 4 Soft-shell eggs, once their contents are removed, easily implode on their own, a n d may therefore pass unaided. 2 Surgical removal is warranted if the egg is lodged in the caudal oviduct or cloaca. An episiotomy should be a t t e m p t e d in these cases. 4 In cases where the egg is severely a d h e r e d to the oviduct wall, the uterus is ruptured, a soft-shelled egg is located cranial to the oviduct, or the egg is ectopic, a ventral laparotomy or possibly, a hysterectomy, is indicated. Once the egg is passed or removed, the bird needs to be followed u p closely because m a n y hens with egg binding or dystocia will lay again soon. Egg binding and dystocia can also recur with future clutches. Historically, medroxyprogesterone was used to stop ovulation after egg binding or dystocia and in cases of chronic egg laying. 2,4 This therapy is considered controversial and is not r e c o m m e n d e d by the author. However, if attempted, progesterone should only be administered after a complete clutch is laid because it may cause soft-shell eggs, mummification, peritonitis, and death. 4 In large doses 36 hours before ovulation, progesterone inhibits
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ovulation and induces follicle atresia. 4 If progesterone is administered 2 to 24 hours before ovulation, it can induce a pre-ovulatory surge of L H and premature ovulation, increasing the risk of egg yolk peritonitis and an ectopic egg. 4 O t h e r side effects ofmedroxyprogegterone include obesity, hepatic lipidosis, weight gain, lethargy, transient or persistent hyperestrogenism, polyuria, and polydipsia. O t h e r complications that occur secondary to egg binding and dystocia include cloacal, oviduct, and uteral prolapse or paralysis, egg yolk peritonitis, scarring or damage to the oviduct, ascending salpingitis or metritis, and abdominal hernias. 4,2
vents aperture while maintaining an exit for urine, urates, and feces. If the cloaca repeatedly prolapses, a cloacalpexy is warrantedJ s If treated promptly, the prognosis for prolapsed tissues is good. 7 Chronic prolapses have a p o o r prognosis for survival of the prolapsed tissue. Surgical d e b r i d e m e n t or possibly a hysterectomy may be required once the patient is stabilized, t9 If an egg is present in the tissues, it must be removed before the prolapse can be replaced. Digital pressure a n d / o r ovocentesis may be necessary in such cases.
Egg Yolk Peritonitis Prolapsed Oviduct Prolapse of the oviduct, uterus, vagina, a n d / o r cloaca can occur secondary to dystocia, normal egg laying, physiologic hyperplasia, or various disease states affecting these tissuesfi 17 Powerful abdominal contractions associated with oviposition, the size of the egg, general debilitation, and malnutrition can all contribute to oviduct prolapse. T h e uterus is most commonly prolapsed, but the vagina, and cloaca may prolapse in part. 4 The caudal oviduct may also prolapse, especially if an egg is present within the tissues. Exposed tissues are susceptible to infection and devitalization and therefore must be treated aggressively. They should be kept moist and clean with warm sterile saline flushes. Immediately before flushing, cloacal cutttire and sensitivity and a CBC and chemistry should also be obtained. Parenteral antibiotics and fluids should be administered. If no egg is present (or if it is easily passed or removed), the tissues are clean, and parenteral antibiotics have been administered, topical sterile lubricant mixed (1:1) with sterile 50% dextrose can be applied to the prolapse tissue to help decrease edema. Some authors prefer topical steroid preparations containing antibiotics or dimethyl sulfoxide gel (DMSO) to help reduce the inflammation in addition to the swelling. 4 The moistened, shrunken tissues are gently replaced with a lubricated swab. Recurrence is c o m m o n with prolapses, and re-replacement should be attempted a few times. If necessary, one stay cruciate suture can be placed laterally on either side of the vent to help prevent reprolapse and allow the tissues to regress in size naturally. This stay suture technique reduces the
Septic egg yolk peritonitis is a term used to describe a highly fatal condition associated with the presence of infection and egg yolk material in the coelomic cavity. 1,2,4Nonseptic yolk peritonitis has a better prognosis because the yolk itself only causes a mild histiocytic response and is gradually reabsorbed if no infection is present. A group of syndromes may contribute to egg yolk peritonitis and include ectopic ovulation secondary to reverse peristalsis, salpingitis, metritis, neoplasia, cystic hyperplasia, r u p t u r e d oviducts, and stress or physical restraint of the egg-laying hen. 4 Acute signs of egg yolk peritonitis include decreased or ceased egg production, depression, anorexia, mild weight loss, a history of broodiness, or recent egg laying. 2,4,2~ Diagnosis and immediate treatment improves prognosis of such cases. Abdominal swelling and ascites are comm o n chronic clinical signs, especially in smaller psittacines. Respiratory distress and sudden death may be associated with these cases. Ascites is rarely seen in macaws. Acute egg yolk peritonitis causes a severe inflammatory response, paralleled by that typically seen with chlamydia, aspergillosis, and osteomyelitis infections, where WBC counts may be greater then 30,000 WBC/txL. Radiography, abdominocentesis, endoscopy, and laparotomy are helpful diagnostic aids. Egg yolk peritonitis is most frequently described in cockatiels, budgerigars, lovebirds, ducks, and macaws, especially scarlet macaws. 19,z~O t h e r syndromes associated with egg yolk peritonitis include egg-related pancreatitis, which may lead to temporary diabetes mellitus, and yolk emboli, which can result in a strokelike syndrome, especially in cockatiels.
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Treatment fo r egg yolk peritonitis depends on the severity of the clinical signs. 2 Traditional medical m a n a g e m e n t of chronic cases includes long-term parenteral antibiotics based on culture and sensitivity and supportive care as needed, including abdominocentesis to reduce abdominal pressure and relieve dyspnea. 2,4 The etiologic agent of egg-related peritonitis is often coliforms, especially Escherichia coli. Yersinia pseudotuberculosis and Staphylococcus spp have been rep o r t e d in association with egg-related peritonitis. Anaerobes and chlamydia have also b e e n implicated. Endoscopy should be p e r f o r m e d in the stabilized patient to assess the severity of the internal pathology associated with egg yolk peritonitis, z Care must be used to minimize ascites before endoscopy or surgery and to position the patient on an incline with the head elevated. If this is not p e r f o r m e d , the bird could drown because the integrity of the airsacs, compartmentalizing the fluid away from the lungs, is the only protection in avian species because they lack a diaphragm. If an excessive a m o u n t of yolk, an inspissated egg, or adhesions exist, then surgery, consisting of a laparotomy with abdominal flushing, is indicated in the stabilized patient. 2,4 Surgical treatment of scarlet macaws has been successful. a9 Prognosis is d e p e n d e n t on p r o m p t detection and early treatment. 2,4 Traditionally it has been believed that most cases resolve with medical therapy alone when detected early in the acute stage. However, chronic egg yolk peritonitis remains the most c o m m o n fatal obstetrical condition in avian species. 1,2,4
Chronic Egg Laying Chronic or excessive egg laying occurs when a hen has repeat clutches, regardless of the presence of a natural mate or the p r o p e r breeding season, or when she lays larger-then-normal clutch sizes. 2,4 T h i s p h e n o m e n o n occurs commonly in cockatiels, budgerigars, and lovebirds, and infrequently occurs in hand-raised psittacine hens that are imprinted on humans. 2,4 The etiology of excessive or chronic egg laying is multifactorial. Malnutrition, genetics, sexual stimulation, photoperiod, and the presence of eggs in their nest, for example, all directly or indirectly affect the bird's h o r m o n a l balance, and ultimately, egg laying. Excessive or chronic egg laying leads to calcium deficiency,
and eventually egg binding, osteoporosis, and severe malnutrition. 2 Malnutrition resulting directly from a p o o r diet, coupled with the calcium depletion of egg laying, exacerbates this phenomenon. As previously mentioned, genetics is known to be responsible for the occurrence of this syndrome in cockatiels, budgerigars, and lovebirds. 2 Sexual stimulation induced by toys, nest boxes, h u m a n beings, inappropriate mates, or natural mates should be eliminated. Decreasing the p h o t o p e r i o d to 8 to 10 hours of light per day interrupts the h o r m o n a l balance, ceasing egg production. The eggs of an excessive or chronic egg layer should be left in the nest or replaced with artificial ones because an empty nest stimulates the h e n to lay again, exacerbating the problem.Z, 4 Clinical signs attributable to end-stage chronic egg laying, in addition to excess egg production, include weight loss and dehydration secondary to chronic regurgitation, feather loss and dermatitis around the vent secondary to masturbation, and abnormal egg production, oviduct inertia, muscular weakness, and pathological fractures secondary to chronic calcium depletion. 2,4Unfortunately, these late signs are typically the first ones noted. Acute or early clinical signs include repetitive or increased frequency of egg laying, increased numbers of eggs layed, and excessive broodiness. These signs are particularly noticeable in detei~minant layers who will normally only lay a set n u m b e r of eggs per clutch regardless of removal or destruction, ie, budgerigars. The majority of parrots are believed to be indeterminant layers who will continue to lay after egg removal or destruction until they recognize the correct n u m b e r of eggs in their clutch. Treatment of chronic or excessive egg laying includes addressing malnutrition, beginning medical/pharmacological treatment, and potentially salpingiohysterectomy. 2 Nutritional a n d / o r vitamin supplementation should be addressed in all cases. Pharmacological medical m a n a g e m e n t of chronic egg layers is controversial and varied. Medroxyprogesterone injections or implants have historically been used in cases of chronic egg laying to interrupt the laying/ovulatory cycle. However, this practice is controversial owing to various side effects including obesity, hepatic lipidosis, weight gain, lethargy, polyuria, and polydipsia. 4,19,22
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As previously mentioned, progesterone should only be administered after a complete clutch is laid. In the case of the chronic egg-laying cockatiel with ascites and nonseptic egg yolk peritonitis, some authors have advocated the use of IM m e d r o x y p r o g e s t e r o n e acetate and dexamethasone. s The side effects of m e d r o x y p r o g e s t e r o n e acetate are numerous, and although they do have a place in avian medicine, they should be used with caution. D e x a m e t h a s o n e should also be used with caution; side effects include i m m u nosuppression, elevated liver enzymes, polyuria, polydipsia, and diarrhea. 2a Oral a n d parenteral testosterone have also b e e n administered in an a t t e m p t to i n t e r r u p t the ovulatory cycle, with varied success. 4 Long-acting leuprolide acetate (Lupron; TAP Pharmaceuticals, Deerfield, IL), a superactive gonadotropin-releasing h o r m o n e (GNRH) has b e e n safely used to reversibly prevent egg laying in cockatiels. 24,25 A p o t e n t G N R H agonist, Lupron, causes pituitary shut down when sustained at high levels over time. Cockatiels injected every 18 days with 100 b~g/kg cease chronic egg laying. 25 Budgerigars n e e d to be injected every 12-14 days with the same dose to achieve the same effect. 25 It has b e e n suggested by some authors that the L H activity of h u m a n chorionic gonadotrophin (HCG) administered at the appropriate stage of follicular d e v e l o p m e n t may cause follicular atresia and therefore may be used as a means to control ovulation. 26 Doses of 500 to 1000 I U / k g IM are generally effective but may n e e d to be r e p e a t e d every 3 to 6 weeks. 26 Ultimately, only a salpingiohysterectomy will stop a chronic egg layer. This p r o c e d u r e is generally considered safe in most m e d i u m - to large-sized psittacines and is also possible in cockatiels, budgies, and lovebirds for skilled surgeons. If left untreated, chronic or excessive egg laying can lead to egg binding, osteoporosis, and severe' malnutrition; thus, preventative medicine and client e d u c a t i o n is very i m p o r t a n t in the t r e a t m e n t of this condition. 2
Oviduct Impaction An impacted oviduct is usually distended and contains m u c h caseous material and misshapen, partially formed, or r u p t u r e d eggs. Oviduct impactions are often associated with salpingitis but
can also occur after metritis, egg binding, or tumors. 4 Cockatiels, canaries, and budgerigars are c o m m o n l y affected, but oviduct impaction has also b e e n r e p o r t e d in African Grey Parr o t s . 17'27"29 Salpingitis and oviduct impaction are m o r e c o m m o n l y associated with older birds. 1 Causes of oviduct impactions include excess mucin or albumin secretion secondary to cystic hyperplasia or inspissated egg material in the m a g n u m . 4 Eggs can impact in the distal oviduct if they are soft or abnormally shaped or even if they are normal. 4 Clinical signs may be mild or could include cessation of egg production, debilitation, constipation, diarrhea, a pasted vent, diffuse or unilateral (usually left side) abdominal swelling, and anorexia. 4 F u r t h e r m o r e , the bird may not be able to walk or fly. Radiology and ultrasound are useful diagnostic aids. However, endoscopy, laparotomy, or necropsy are usually n e e d e d for a definitive diagnosis. T r e a t m e n t includes cloacal/oviduct culture a n d sensitivity, long-term parenteral antibiotics, and, in most cases, salpingiotomy to clean out a n d debride the oviduct. Possibly, a salpingiohysterectomy may be needed, as the integrity of the uterine wall may not allow for healing after salpingiotomy. 4
Oophoritis Oophoritis, or an infection Of the ovary, is a reflection of the patient's health status and is frequently associated with systemic bacterial disease and sepsis, a~ T h e condition is serious and results in peritonitis and potentially death if not identified early and treated. Clinical signs include depression, anorexia, chronic wasting, and sudden death. 3~ Diagnostics include t h o r o u g h endoscopic evaluation, taking care to identify wrinkled, black, enlarged, firm, hemorrhagic, and attached or free coagulated ovum. 4 T h e r a p y includes supportive care and parenteral antibiotics as indicated by cloacal culture and sensitivity. 4
Salpingitis and Metritis Salpingitis occurs most c o m m o n l y in adult hens but is also seen in younger birds. T h e infection may be descending, secondary to air sacculitis, or p n e u m o n i a , or ascending, f r o m the distal uterus, vagina, or cloaca. Salpingitis has
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been associated with oviductal impaction, especially in passerines as well as with foreign bodies or excessive abdominal faL 2,8,31,32 E. coli is the most c o m m o n isolate, but Streptococcus spp, Mycoplasma gallisepticum, Salmonella spp, and Pasteurella multocida have b e e n implicated from various species. 4,33 Metritis is localized within the uterine portion of the oviduct and is typically a sequela to dystocia, egg binding, or chronic oviduct impaction. 4 One clinical sign associated with metritis is abnormal thickness, shape, and size o f eggs. Infections can occur in embryos or neonates secondary to metritis. Metritis may also cause egg binding, uterine rupture, peritonitis, and septicemia. 4 E coli is commonly isolated, but other coliforms have also been implicated. Severely affected birds may have an enlarged a b d o m e n and a palpable turgid uterus. 4 Radiographs typically show p o o r coelomic cavity detail. However, ultrasound is an excellent tool for evaluating oviduct size, shape, and contents in most medium- to large-sized psittacines. Clinical signs for both salpingitis and metritis may include weight loss, abdominal enlargement, and depression. 4 A discharge from the cloaca may also occur, and it is important to do cultures and sensitivities. CBC usually shows a severe leucocytosis. Treatment includes supportive care, long-term antibiotics, and retrograde direct or indirect oviduct flushing. Nonresponsive cases may n e e d surgery. Necrotic tissue should be removed via laparotomy and opening of uterus, and exudates and egg material should be removed by n o r m o g r a d e flushing or irrigation.
Ectopic Eggs Ectopic eggs result from the failure of the infundibulum to enguIf an ovum, a r u p t u r e d oviduct, or a discontinuous o v i d u c t . 4 Causes of infundibulum failure include exuberant reverse peristalsis, oviduct fat, trauma, or disease. 4 Physical restraint may also cause ectopic ovulation, therefore mating hens in season should be examined only when absolutely necessary. 3~ Ectopic ovulation occurs frequently in birds, and reportedly 28.6% in one study of nine avian orders. 1 Oviduct rupture occurs secondary to multiple pathologic conditions affecting the oviduct including large oddly shaped eggs, severe impac-
tion, egg binding, cystic hyperplasia, salpingitis, or neoplasia. Diagnosis is based on clinical signs, radiography, and ultrasound. Affected hens are depressed, lose weight, have a penguinlike stance, and have ascites. Removal or repair of damaged oviductal tissue is imperative. 4 The patient should be stabilized with rest, fluids, calcium, and broad spectrum antibiotics, pending cloacal culture and sensitivity. If the oviduct is repairable, it is flushed with warm saline and dilute chlorehexidine and surgically debrided as necessary. 4 The coelomic cavity is flushed with warm saline during oviductal surgery. Hence, eggs, caseated material, a n d / o r egg parts are removed.
Cystic Hyperplasia of the Oviduct Cystic hyperplasia of the oviduct has been reported in psittacines, especially budgerigars25 The oviduct is typically dilated with white or brown mucoid fluid and white to beige creamy masses. Clinical signs include ascites, abdominal distention, and respiratory distress. Diagnosis is based on abdominal palpation, clinical signs, radiology, and ultrasound. Treatment entails supportive care, antibiotics, based on cloacal culture and sensitivity, and salpingiohysterectomy is curative, as the problem tends to recur.
Congenital Defects Rudimentary right oviducts when present can develop cysts of significant size that could contribute to egg binding. This condition has been identified in the budgerigar. 1 Treatment is cyst removal when possible. Discontinuous or atretic oviducts have been identified in domestic fowl and can lead to ectopic eggs a n d / o r egg yolk peritonitis. 4
Neoplasia Ovarian neoplasia is more c o m m o n than oviduct neoplasia in psittacinesY Both have been described with increased frequency in the budgerigar. 27 Cloacal carcinomas are infrequent, characterized by dysplastic pleomorphic cells with bizarre mitosis. These tumors are transmurally invasive and hence may be associated with sclerosing fibroplasia, a4 Ovarian tumors can enlarge to one third the bird's body weight causing
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massive o r g a n d i s p l a c e m e n t . H e r n i a t i o n , ascites, a n d cysts a r e f r e q u e n t s e q u e l a e to n e o p l a s i a o f t h e o v a r y a n d oviduct. T h e m o s t s i g n i f i c a n t clinical sign s e c o n d a r y to a b d o m i n a l e n l a r g e m e n t is d y s p n e a , b u t c e r e c o l o r c h a n g e s a r e also o b s e r v e d in t h e b u d g e r i g a r , as is u n i l a t e r a l o r b i l a t e r a l paresis o r paralysis. D i a g n o s i s i n c l u d e s p a l p a t i o n , r a d i o g r a p h y , a n d u l t r a s o u n d b u t is b e s t b a s e d o n l a p a r o t o m y , biopsy, with o r w i t h o u t mass excision, a n d h i s t o p a t h o l o g y . 4 C o m m o n l y reported ovarian tumors include adenocarcinomas, a d e n o m a s , g r a n u l o s a cell t u m o r s , l i p o m a s , f i b r o s a r c o m a s , a n d c a r c i n o m a t o s i s . O v i d u c t a l tumors include adenomatous hyperplasia, adenocarcinomas, adenomas, and carcinomatosis. 4
Cloacal Pathology Cloacitis, cloacal strictures, cloacaliths, c h r o n i c cloacal p r o l a p s e s , cloacat p a p i l l o m a s , c l o a c a l h y p e r p l a s i a o r a d e n o m a t o u s polyps, a n d excessive c l o a c a l fat, s u r r o u n d i n g f e a t h e r s , o r p e n d u lous a b d o m i n a l l i p o m a s c a n all physically interfere with egg-laying a n d c o p u l a t i o n . T M E a c h c o n d i t i o n m u s t b e a d d r e s s e d medically, with a full w o r k - u p , a n d , w h e n necessary, c o r r e c t i v e s u r g e r y s h o u l d b e p e r f o r m e d . Cloacaliths, strictures, p r o l a p s e s , a n d p a p i l l o m a s o f t e n r e q u i r e surgical i n t e r v e n t i o n . C l o a c a l i t h r e m o v a l is o f t e n rewarding, whereas strictures are often complex a n d difficult to resolve. C l o a c a l p a p i l l o m a s p r e sent a unique and potentially infectious problem. A l t h o u g h o f u n k n o w n o r i g i n , a virus is s u s p e c t e d , a n d i s o l a t i o n o f i n f e c t e d i n d i v i d u a l s is r e c o m m e n d e d . 4 However, eggs o f p a p i l l o m a positive Blue a n d G o l d Macaws, p u l l e d at day o n e a n d artificially i n c u b a t e d , have b e e n s h o w n to p r o d u c e h e a l t h y chicks in o n e s t u d y o v e r a period of 7 yearsY
Conclusion M a n y p r o b l e m s e n c o u n t e r e d in avian obstetrics n e e d i m m e d i a t e a t t e n t i o n , h e n c e p r o p e r i d e n t i f i c a t i o n a n d t r e a t m e n t is i m p e r a t i v e . T h e classic " p r o b l e m - o r i e n t e d a p p r o a c h , " c o u p l e d with k n o w l e d g e o f t h e c o m m o n o b s t e t r i c a l diseases a n d p r e v e n t a t i v e m e d i c i n e skills, s h o u l d facilitate early detection and appropriate therapy. 2 O f t h e c o m m o n p r o b l e m s in avian o b s t e t r i c a l m e d i c i n e d i s c u s s e d previously, e g g
binding, egg yolk peritonitis, and chronic egg laying a r e m o s t f r e q u e n t l y e n c o u n t e r e d . Because obstetrical problems are multifactorial a n d p r o g n o s i s varies b e t w e e n individuals, t h e d e c i s i o n to p r o c e e d with d i a g n o s t i c s o r i m m e d i ately c o m m e n c e e m e r g e n c y s u p p o r t i v e treatm e n t is case b a s e d . H e n c e , n o t o n l y is p r o p e r d i s e a s e d e t e c t i o n i m p o r t a n t , b u t t h e avian clinic i a n m u s t b e sensitive to e a c h p a t i e n t ' s indiv i d u a l level o f debility.
References 1. Keymer IF: Disorders of the avian female reproductive system. Avian Pathol 9:405-419, 1980 2. Speer B: Clinical reproductive avian medicine, in Foundations in Avian Medicine. Proceedings of the Association of Avian Veterinarians. Philadelphia, PA, 1995, pp 23-33 3. Astheimer LB: Long laying intervals: A possible mechanism and its applications. Auk 102: 401-409, 1985 4. Joyner KL: Theriogenology, in Ritchie BW, Harrison GJ, Harrison LR (eds): Avian Medicine: Principles and Application. Lake Worth, FL, Wingers, 1994, pp 748-804 5. King SA, McLelland J: Female reproductive system, in King SA, McLelland J (eds): Birds: Their Structure and Function. Philadelphia, PA, Bailliere Tindall, 1984, pp 145-174
6. Harrison GJ: Reproductive medicine, in Harrison GJ , Harrison LR (eds) : Avian Medicine and Surgery. Philadelphia. PA, Saunders, 1986, pp 620-633 7. HashlotJ: Disease of the female reproductive organs of pet birds. J Small Anita Pract 32:313-320, 1966 8. Rosskopf WJ, Woerpel RW: Egg binding in caged and aviary birds. Mod Vet Pract 65: 437440, 1985 9. Smith RE: Hysterectomy to relieve reproductive disorders in birds. Avian Exotic Pract 2:40-43, 1985 10. Hochleithner M, Lechner C: Egg binding in a budgerigar caused by a cyst of the right oviduct. Assoc Avian Vet Today 2:136-138, 1988 11. Johnson AL: Reproduction in the female, in Sturkie PD (ed): Avian Physiology (ed 4). New York, SpringerVerlag, 1986, pp 403-431 12. Quessenberry KE, Hillyer EV: Supportive care and emergency therapy, in Ritchie BW, Harrison GJ, Harrison LR (eds) : Avian Medicine: Principles and Application. Lake Worth, FL, Wingers, 1994, pp 382-416 13. Hudelson S, Hudelson P: Egg Binding, hormonal control, and therapeutic considerations. Compend Contin Educ 15: 427-432, 1993 14. Hudelson S: Personal communication, February 1996 15. Hudelson KS, Hudelson P: A brief review of the female avian reproductive cycle with special emphasis on the role of prostaglandins and clinical applications. J Avian Med 10:67-74, 1996 16. Fudge AM, Van Sant F, Zantop D: Personal communication,July 1996 17. BeachJE: Diseases of budgerigars and other cage birds: A summary of postmortem findings. Vet Rec 74:63-68, 1962 18. Rosskopf WJ, Woerpel RW: Cloacal conditions in pet birds, with a cloacalpexy update. Proceedings of the
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Association of Avian Veterinarians. Seattle,WA, 1989, pp 213-231 Rosskop'fWJ, Woerpel RW: Pet avian obstetrics. Proceedings of the First International Conference of Zoological and Avian Medicine, Oahu, HI, 1987, pp 213-231 Speer BL : Non-infectious disease, in AbramsonJ, Speer BL, ThompsonJB (eds): The Large Macaws: Their Care, Breeding and Conservation. Fort Bragg, CA, Raintree Publications, 1995, pp 316-333 Rosskopf WJ, Woerpel RW: Psittacine conditions and syndromes. Proceedings of the Association of Avian Veterinarians. Phoenix, AZ, 1990, pp 432-459 Harrison GJ: Progesterone implants in cases of chronic egg laying in cockatiels. Proceedings of the Association of Avian Veterinarians. Seattle, WA, 1989, pp 6-10 Ritchie BW, Harrison, GJ: Formulary, in Ritchie BW, Harrison GJ , Harrison LR (eds): Avian Medicine: Principles and Application. Lake Worth, FL, Wingers, 1994, pp 457-478 Millam JR, Finney H: Leuprolide acetate can reversibly prevent egg laying in cockatiels. Proceedings of the Association of Avian Veterinarians, Nashville TN, 1989, pp 46 Orosz S: Personal communication, February 1996 Lighffoot T: Personal communication, February 1996 Blackmore DK, CooperJE: Diseases of the reproductive system, in Petrak ML (ed): Diseases of Cage and Aviary Birds (ed 2). Philadelphia, PA, 1982, pp 458-467
28. Degernes L: Chronic oviduct obstruction and salpingitis in an African grey parrot. Proceedings of the Association of Avian Veterinarians. New Orleans, LA, 1992, pp 156-157 29. Degernes L: Abdominal mass due to chronic salpingitis in an African grey parrot (Psittacus erithacus). Vet Pad US 34: 24-28, 1993 30. Peckham MC: Reproductive disorders, in Biester HE, Peckham MC (eds): Diseases of Poultry(ed 5). Ames, IA, Iowa State University Press, 1965, pp 1201-1205 31. Keymer IF: The diagnosis and treatment of some diseases of seed-eating passerine birds. Mod Vet Pract 40:30-34, 1959 32. Reece RL: Reproductive diseases, in Burr E (ed): Companion Bird Medicine. Ames, IA, Iowa State University Press, 1987, pp 89-100 33. Gross WB: Colibacillosis, in Calnek BW, Barnes HJ, Beard CW, et al (eds): Diseases of Poultry (ed 9). Ames, IA, Iowa State University Press, 1991, pp 138-144 34. Latimer KS: Oncology, in Ritchie BW, Harrison GJ , Harrison LR (eds): Avian Medicine: Principles and Application. Lake Worth, FL, Wingers, 1994, pp 640-672 35. Bond M: Utilizing papilloma infected blue and gold macaws (/Era araruna) in a breeding collection. Proceedings of the Association of Avian Veterinarians. Philadelphia, PA, 1995, pp 469472