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Review of Ovarian Abnormalities in the Mare

Pa tric k M. McCue , DVM, Ph D, Dipl. ACT

The cli nical signs and t reat ment s of ovari an abnormal i t ies i n t h e ma re a re revi ewed. Cli nical

techniques that may be used in the diagnosis and differentiation of ovarian abnormalities are also

presented. Author’s address: Dept. of Clinical Sciences, Colorado Stat e University, Ft. Collins, CO

80523. 1998 AAEP.

1. Introduction

Path ologic conditions of the equine ovary can bedivided into abnormalities that cause the ovaries tob ecom e la r ge r t h a n n or m a l, t h a t ca u s e t h e m t obecome smaller than normal, or that cause an alter-ation in normal ovarian physiology or function.The purpose of this paper is to review the clinicals ig n s , d ia g n os t i c p r o ce d u r e s, a n d t r e a t m e n t s of ovarian abnormalities in the mare.

2. Materials and Methods

This paper reviews scientific and clinical literaturecon ce r n in g ov a r ia n a b n or m a l it i es i n t h e m a r e .Clinical techniques that may be used in the diagno-sis and differentiation of ovarian abnormalities arelisted in Table 1.

3. Results

A. Normal Ovaries

Equine ovaries are kidney shaped and have a promi-nent depression on their ventral border, the ovula-tion fossa, through which all ovulations take place.The size of the ovaries varies with season, age, andstage of the estrous cycle.1,2 A majority of the ovaryis covered with viscera l peritoneum or serosa. Theovulation fossa is l ined by germinal epithelium.

Adipose tissue and adrenocortical nodules are com-

monly foun d un der t he serosal sur face of th e equineovary.2 Tun ica albuginea, a th ick connective tissuelayer, is locat ed beneath th e serosa. Ovarian archi-t e c t u r e o f t h e h o r s e i s u n i q u e i n t h a t t h e c o r t i c a lzone, which contains the follicles and corpora lutea,i s l oca t e d i n t h e i n t er i or of t h e ov a r y, w h il e t h emedullary or vascular zone is located in t he su perfi-cial region.1

Follicles are composed of two main cell types, i.e.,granulosa an d theca cells. Granu losa cells l ine theinside of the follicle. The oocyte is surr oun ded by alayer of granulosa cells called the cumulus oophorusand is atta ched to th e interna l follicular wall at theh i ll ock . T h e ca ce ll s s u r r o u n d t h e ou t s id e of t h e

follicle and are separated from granulosa cells by abasement membran e. Granu losa cells produce theprotein hormone inhibin and, in conjunction withtheca cells, produce estradiol. Theca cells are re-sponsible for the production of androgens.

Ovulation occurs in response to a surge of luteiniz-ing hormone secreted by th e ant erior pituita ry. Therupture of the follicle results in hemorrhage fromb lood v es s el s i n t h e t h e ca a n d for m a t i on of a nintermediate structure, t he corpus hemorrhagicum.A corpus luteu m su bsequently forms from t he corpushemorrhagicum following invasion of granulosa and

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NOTES

AAEP PROCEEDINGS 9 Vol. 44 / 1998 125

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Proceedings of the Annual Convention of the AAEP 1998



l u t ea l ce ll s. L u t e in i za t i on of t h e g r a n u los a a n dtheca cells results in the development of large an dsmall luteal cells, respectively. The corpus luteumof th e nonpregnan t ma re secretes pr ogesterone untilprostaglandins released by th e endometrium causedestruction of the luteal cells, or luteolysis.

B. Enlarged Ovaries

The different ial diagnosis for un ilater ally or bilater-ally enlarged ovaries in the mare includes pathologic

conditions such as ovarian tumors and ovarian hema-tomas and physiologic conditions such as the ovarianenlargement tha t n ormally occur s dur ing pregnan cy.

1. Granulosa Cell Tumor

The most common ovarian tumor in t he ma re is thegranulosa cell tumor (GCT).3 Granu losa cell t u-mors a re almost always un ilateral, slow growing,and benign. An examination of the affected ovaryby using tran srectal ultra sonograph y often r eveals amulticystic or honeycombed structure (Fig. 1), butthe tumor may also present as a solid mass or as asingle large cyst (Figs. 2 and 3). The contra lateralovary is usually small and inactive, although mares

with a GCT on one ovar y and a functiona l contra lat-eral ovary have been reported.4 Behavioral abnor-malities such as prolonged a nestrus, aggressive orstallionlike behavior (Fig. 4), and persistent estrusor nymphoma nia m ay be expressed in affected mar es.

Granulosa cell tumors are hormonally active, andclinical diagnostic assays for the detection of a GCTinclude t he measurement of inhibin, testosterone,and progesterone (see Appendix A for endocrinelaboratories).5, 6 I n h ib in i s e le va t e d i n a p p r ox i-mately 90% of the mares with a GCT. 5 It has beenhypothesized that inhibin produced by the GCT isresponsible for the inactivity of t he contra lateralovary through the suppression of pituitary follicle-

stimulating hormone release. Serum testosteronelevels ma y be elevated if a significant theca cellcomponent is present in th e tu mor (i.e., a gra nu losa-theca cell tu mor, or GTCT). Testosterone is ele-vated in approximately 50–60% of a ffected maresand is usu ally associated with stallionlike behavior.Progesterone concentrations in mares with a GCTa r e a l m os t a l wa y s b el ow 1 n g /m l , s i n ce n or m a lfollicular development, ovulation, and corpus lu-teum formation do not occur.

Therefore, measurements of inhibin levels 0.7ng/ml, testosterone levels 50–100 pg/ml, and proges-

terone levels of 1 ng/ml are suggestive of a granu-losa cell tumor in a nonpregnant mare (Table 2).

Granulosa cell tumors are usually surgically re-moved if the tumor affects follicular development onthe contra lateral ovary, causes behavioral abnor-ma lities, or is a source of colic. Sur gical appr oachesfor tumor removal include colpotomy, flank andventral midline laparotomy, and laparoscopy.

Ovulation from the remaining ovary will occura p p r ox im a t e ly 6 –8 m on t h s a ft e r t u m o r r e m ov a l.Attempts at inducing follicular development and

Table 1. Procedures Used to Evaluate Ovarian Abnormalities

Clinical Techniqu e

Behavioral observation

Physical examinat ion

Palpation per rectum

Ultrasonography per rectum

Hormone ana lysis

Karyotyping

Fig. 1. Sonograph of a GCT in a mare.

Fig. 2. GCT composed of multiple small cysts.

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126 1998 9 Vol. 44 9 AAEP PROCEEDINGS





ovulation in t he r emaining ovary within 1 monthafter tu mor removal by the administr ation of gonado-tropin-releasing hormone (GnRH) has not been suc-ce s sfu l . H o we ve r, t h e a d m i n is t r a t i on of e q u in efollicle-stimulating hormone, in the form of equinepituitar y extract, ha s been su ccessful in indu cing anov u la t i on fr om t h e con t r a l a t e r a l ov a r y a ft e r t h es u r gica l r e mova l of a G CT t h a t r e su lt e d in apregnancy.a

2 . C ys t ad en om a

The most common tumor of the surface epithelium of the equine ovary is the cystadenoma. Cystadeno-mas occur unilaterally, a nd the contra lateral ovaryis n or m a l. T h e u lt r a s on og r a ph i c a p p e a r a n ce of the affected ovary may include one to many cyst-l ik e s t r u c t u r e s (F i g. 5 ). I n g en e r a l, t h e s e t u m o r sa r e r a r e a n d b e n i g n a n d a r e n o t c o n s i d e r e d t o b ehormonally active, a lthough reports of ma res withcystadenomas with elevated plasma testosteroneconcentr ations ha ve been ma de.3,7

The treatm ent of choice for an ovarian cystad-enoma is sur gical removal. The decision to remove

the affected ovary does not h ave to be m ade imm edi-ately, as t he t umor is slow growing and ha s not beenr e p or t e d t o m e t a s t a s i ze . H ow ev er , i f t h e t u m o rd oe s con t i n u e t o e n la r g e, t h e m a r e m a y e xh i bi tepisodes of abdominal pain.

3. Teratom a and Dysgerminoma

Te r a t om a s a n d d ys ge r m in om a s a r e r a r e ov a r ia ntu mors of germ cell origin.8,9 Terat omas a re consid-

ered to be benign, while dysgerminomas are poten-tially malignant. Both ar e unilateral, hormonallyinactive, and associated with normal contralateralovaries. Germ cell tumors may contain h air, bone,muscle, an d other t issues (Fig. 6). They do not altert h e b e h a v i o r o f t h e m a r e a n d d o n o t i n t e r r u p t t h eestr ous cycle.

The treatm ent of choice for germ cell t umors iss u r g ica l r e m ov a l. T h is i s e s p eci a ll y t r u e for t h ed ys ge r min om a , b eca u s e of it s p ot en t ia l formetastasis.

4 . O v ar ia n H em a t o m a

Hematomas are one of the most common causes of unilatera l ovarian enlargement. 10,11 Hematomas re-sult from excessive hemorrhage into the follicularlumen following ovulation, and they are essentiallyg r ea t l y e n la r g e d cor p or a h e m or r h a g i ca (F i g. 7 ).The contr alateral ovary is n ormal in size and func-tion, and t he mar e continues to cycle normally. Nobehavioral abnormalities are noted and endocrinepatterns of the mare a re normal.

H e m a t om a s of t h e ov a r y u s u a l l y d o n o t r e qu i r etreatment . The hematoma will gradually reduce ins iz e o ve r a p e r iod of s e ve r a l w e e k s, a n d i n m os ti n st a n c es t h e ov a r y r e t u r n s t o n or m a l fu n c t ion .However, occasiona lly a hema toma may destroy theovarian germinal tissue, rendering the affected ovarynonfunctional.

5. Cystic Ovaries

The presence (or absence) of cystic ovaries in themar e, as described in dairy catt le, ha s been a subjectof debate for years. Persisten t anovulatory follicles

Fi g. 5. Ovarian cyst adenoma from a mare.

Table 2. Hormone Concentrations in the Normal Nonpregnant Mare

H or m on e Nor m a l Ra n ge

In h ibin 0.1–0.7 n g/m l

Test ost er on e 20–45 pg/m l

Progesterone

est rus 1 ng/ml

diestrus 1 ng/ml

Fig. 3. GCT composed of a single large central cyst.

Fig. 4. Mare with a GCT, exhibiting stallionlike behavior.

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d o o c c u r i n t h e m a r e a n d a r e d i s c u s s e d i n a l a t e rsection.

A case of bilateral polycystic ovaries was recentlyd ia g n os e d i n a 6 -y ea r -ol d A n d a lu s ia n m a r e p r e -sented to Colorado Stat e Un iversity. The ovarieswere each approximately 15 cm in diameter and hadremained enlarged for almost 2 years. Ultrasono-g r a p h ic e va l u a t ion s a n d m e a s u r em e n t s of s e r u mhormone concentrations were performed every 1–3months. A laparoscopic ovarian biopsy was eventu-ally perform ed on each ovary, and a h istologic diagno-sis of polycystic ovar ies was ma de independ ently bypathologists at two institutions. The ovaries weresubsequ ently removed, an d a fur th er histologicevalu -ation confirmed the previous diagnosis of polycysticovaries.

Cysts within the region of the ovulation fossa (Fig.8 ) a n d cy st s a d ja ce n t t o a n d w it h i n t h e ov id u ct a ltissue are common in the mare and generally arisefrom st ru ctu ral remn an ts of the mullerian or wolf-fi a n d u ct s . F os s a cy st s a n d p a r ov a r ia n cy st s m a ybe found in a high percenta ge of mares a s incidenta lfindings. These cysts are generally not associated

with reduced fertil ity u nless they obstruct t he pro-cess of ovulation or oocyte tra nsport into and thr ought h e ov id u ct . N o t r e a t m e n t i s n e ce ss a r y f or fos s a

cy st s or p a r ov a r ia n (fi m b r ia l ) cy st s t h a t a r e n otinterfering with ovulation or oocyte transport.

6. Ovarian Enlargem ent During Pregnancy

Pregnant mares h ave bilateral ovarian enlargementafter secondary corpora lutea begin to form at ap-proximately day 40.1 P r e gn a n t m a r e s m a y s h owestrus, aggressive behavior, or stallionlike behavior.Testosterone concentr at ions increase t o great er t ha n100 pg/ml by days 60–90 of pregnancy and reachpeak concentra tions at approximately day 200 of pregnan cy (Fig. 9).12 Testosterone concentra tionssubsequently decline t o basal levels by the t ime of foa l in g . T h e m a j or s ou r ce of t e s t os t e r on e i s t h e

fetal gonads, which atta in a size tha t is larger t hanthe ovary of the mare at 7–8 months of gestation.The decline in size of the fetal gonads is associatedwith a decrease in t estosterone concentr at ions in t hep r e gn a n t m a r e . P r e gn a n c y m u s t b e r u l ed ou t b e -

Fi g. 6. Ovari an t erat oma from a mare.

Fi g. 7. Ovarian hemat oma from a mare.

Fig. 8. Subepithelial inclusion (ovulation fossa) cysts from a

m a r e .

Fig. 9. Graph of testosterone concentr ation in a pregnant ma re.

MARE SESSION






fore considering th e possibility of a gr anu losa celltumor in a mare with bilaterally enlarged ovaries,elevated testosterone, a nd sta llionlike beha vior.

N o t r e at m e n t i s w a r r a n t ed for t h e b eh a vior a lch a n g e s t h a t m a y occu r s e con d a r y t o t h e n or m a lphysiologic increase in testosterone during preg-n a n c y. M a n a g em e n t p r a ct i ce s s h ou l d b e i m pl e-m en t ed t o e n su r e t h a t a p r egn a n t m a r e w it haggressive or st allionlike beha vior does n ot injure aperson or another horse. The ovaries of the preg-nan t m ar e should obviously not be rem oved.

C. Small Ovaries

The differential diagnosis for bilaterally small orinactive ovar ies in th e mar e include pat hologic condi-tions such as chromosomal abnormalities, EquineCushing’s Disease, exogenous h ormone tr eatm ent,and maln utr ition an d ph ysiologic conditions such a sprepuberty, advanced age, seasonal anestrus, andpostpartum anestrus.

1. Chrom osom al Abnormalities

The normal chromosome number of th e domestichorse (Equus caballus) is 64, and i t consists of 62aut osomes a nd two sex chromosomes.13 The karyo-type of the n ormal mare and stall ion are 64,XX and64,XY, r espectively. Horses of all domestic breedsh ave t he sa m e n u mber, s ize, a n d sh a pe of chromosomes.

Chromosomal abnorma lities, especially of the sexchromosomes, have been associated with infertilityin th e horse. The prevalence of sex chromosomeabnormalities in the mare has been reported to be

3 %. A c h r om os om a l a b n or m a lit y m a y b e s u s-p ect e d in a m a r e of b r ee di n g a g e w it h p r im a r yinfertility an d gonadal hypoplasia.

The most commonly reported chromosomal abnor-mality of the horse is 63,X gonadal dysgenesis, inwhich only a single sex chromosome is pr esent.14

The condition may occur when the sex chromosomepair fails to separate during meiosis, producing onegamete without a sex chromosome and another witht w o s e x ch r o m os om e s . T h e e qu i n e con d i t ion i sa n a l og ou s t o Tu r n e r ’s s yn d r om e i n h u m a n s . T h e63,X (or XO) condition ha s been detected in mostdomestic horse breeds, including draft and minia-ture breeds.

Horses with gonadal dysgenesis develop as pheno-t y pi c fe m a le s b eca u s e of t h e a b s en ce of a Y s e xchromosome. Affected horses are often small in sizefor their age and breed, have small ovaries lackingfollicular development , an d h ave endometr ial glandh y pop la s ia (F i g. 1 0 ). T h e u t e r u s a n d ce r vi x a r egenerally small and flaccid. The external genitaliais female, but the vulva may be smaller than normaland ther e is no clitoral hypertr ophy. XO mar es mayexhibit anestrous or irregular estrous behavior andoccasionally stand t o be mated. True XO mares arecon s id e r ed t o b e s t e r il e. H ow ev er , m a r e s w it h a

mosaic or chimeric k ar yotype (63,XO/64,XX) are notalways small in sta tu re an d some ha ve been reportedto produce a foal. Mosaic mar es accoun t for approxi-mately 15–30% of all cases of gonadal dysgenesis.Numerous other chromosomal abnormalities h avealso been report ed in the ma re.15

Chromosome ana lysis (karyotyping) can be per-formed on any t issue with actively dividing cells.

A fresh blood sample collected into acid citratedextrose or heparin may be sent by overnight courierto a laboratory specializing in animal karyotyping(see Appen dix A).

An examination of peripheral blood smears for sexchromosome ap penda ges, or dr um sticks, on polymor-phonuclear neutrophils (PMN’s) can be u sed a s ascreening procedure to detect a reduced n umber of chromosomes. Drumsticks appear as a lobe on th enucleus of PMN’s and are present in approximately10% of PMN’s from n ormal ma res a nd are absent installions a nd geldings. An examination of periph-eral blood smears will reveal an absence of drum-sticks in XO ma res.

No treatments are possible to correct a chromo-somal abnormality.

2. Age-Related Ovarian Dysfunction

Ovulatory dysfun ction has been identified as a cau seof subferti l i ty in mares approximately 20 years of age or older. Older mares may have a longer inter-ovulatory interval than younger mares because of alonger follicular pha se.16,17 A l e n g t h e n i n g o f t h efollicular phase in association with elevated gonado-tropin concentra tions may indicate impending repr o-d u ct i ve s e n e sce n ce i n ol d er m a r e s .18 Completeovulation failure or ovarian senescence has beenob se rve d in a ge d m a r e s a n d m a y b e d u e t o a n

insufficient nu mber of primordial follicles. In a ddi-tion, older mares may experience a delay in theirinitial ovulat ion of th e year by an a vera ge of 2 weeks.

No effective treatments are currently available inthe mare for promoting follicular growth in senes-cent ovaries. Pr edisposing factors for subfertility inolder mares such as poor perineal conformation andineffective uterine clearance should be addressed.

3. Exogenous Hormone Treatm ent

Anabolic steroid administration may effect both es-t r ou s b eh a v ior a n d ov a r ia n fu n c t ion . T h e t r e a t -

F i g. 1 0. R ep r od u ct i ve t r a c t of a m a r e w it h 6 3, XO g on a d a l

dysgenesis.

MARE SESSION






ment of mares with low doses of anabolic steroidsmay cause aggressive or stallionlike behavior, whilehigh doses may inhibit ovarian activity and r esult infailure of follicular development and ovulation.19

The a dministr ation of anabolic steroids t o prepuber-tal fillies ma y result in cli toral hypertrophy. Theuse of anabolic steroids should be avoided in filliesand mar es intended to be used for breeding.

Progestins are commonly given to cycling maresfor the suppression of estrus or synchronization of ov u la t i on . M a r e s m a y con t i n u e t o o vu l a t e d u r i n gprogestin administration, especially if treatment isstarted late in the luteal phase. A high incidence of persistent corpus luteum format ion has been notedfor mares ovulating during progestin treatment.20

4. Equin e Cushin g’s Disease

Mares with hypertrophy, hyperplasia, or adenomafor m a t i on i n t h e p a r s i n t er m e d ia of t h e p it u i t a r y(Equine Cushing’s Disease, or E CD) have been re-ported t o have abn orma l estr ous cycles, infertility, or

both.21,22

T h e m e ch a n i s m s b y w h i ch E C D ca u s er e p r od u ct i ve a b n or m a l it i es h a v e n ot b ee n d e t er -mined. A majority of horses diagnosed with ECDare older, with the average age being approximately20 years. Consequently, the decrease in reproduc-tive efficiency in ma res with ECD m ay be pa rtly du eto advanced age. Possible causes of reproductivea b n or m a l it i es i n m a r e s w it h E C D i n cl u de a n i n -creased production of androgens from the adrenalglan d an d compression of the h ypoth alamu s or ante-r ior p it u it a r y b y t h e e n la r g ed p a r s i n t er m e di a .Both factors ma y lead to a decrease in gonadotropinsecretion and consequently a reduction in ovarianfol li cu l a r d e ve lop m e n t . I n a d d it i on , m a r e s w it h

E C D m a y b e p r ed is p os ed t o u t e r in e i n fe ct i on s .Docum ent at ion of the effects of ECD on r eprodu ctiveperforma nce in the m are is limited.

Clinical signs of ECD include h irsutism a nd a bnor-mal hair-coat shedding patterns, polyuria, polydip-

sia, a nd hyperhidrosis (Fig. 11).23 Diagnostic test s

for ECD include m easurements of serum glucose,

insulin, adren ocort icotropic h ormone (ACTH) and

cor t i s ol l ev el s a n d d e xa m e t h a s on e s u p p r e s s ion ,

ACTH stimulation, and thyrotropin-releasing hor-

m on e r e s p on s e t e s t s . T h e m e a s u r e m en t of s in g le

samples for basal cortisol or ACTH concentrations

are of limited value in the diagnosis of ECD.T h e m e d ica l m a n a g e m en t of E C D i n cl u de s t h e

administration of pergolide mesylate, a dopamine

receptor agonist, at a dosage of 0.5–2 mg q 24 h per

adult horse. Cyproheptadine, a serotonin an tago-

n is t, h a s a ls o b ee n u s ed , b u t it m a y n ot b e a s

efficacious as pergolide. The dose of cyprohepta-

dine is 0.25 mg/kg q 24 h, given once in the morning.

D. Other Ovarian Abnormalities

1. Persistent Corpus Luteum

T h e cor p u s l u t eu m t h a t for m s a ft e r ov u la t i on i s

usually functional for 14–15 days in the nonpreg-nant ma re. Corpora lutea that fail to regress at the

n or m a l t i m e p os t ov u la t i on a r e con s id e r ed t o b e

pathologically persistent.24

Luteolysis, or destruction of th e corpus luteum,

occurs as a result of prostaglandin release from the

endometrium. Occasionally, however, a ma re ma y

fail to regress her corpus luteum spontaneously at

t h e n o r m a l t i m e. T h e m os t c om m on ca u s e s of a

persistent corpus luteum are (1) inadequate prosta-

glan din r elease at days 14–15; (2) ovulations late in

diestrus, resulting in corpora lutea that are imma-

t u r e (5 d a y s o ld ) a t t h e t i m e o f p r os t a g la n d i n

release; (3) embryonic loss after the time of maternalrecognition of pregnancy; and (4) chronic u terine

infections, r esulting in destru ction of the en dome-

t r i u m a n d t h e r e for e a d im i n is h e d p r os t a g la n d i n

release.

I f u n t r e a t e d , t h e cor p u s l u t eu m m a y p e r si st for

2–3 months. This syndrome may be suspected clini-

c a l l y i n m a r e s t h a t a r e n o t e x p r e s s i n g n o r m a l e s -

t r o u s b e h a v ior d u r i n g t h e p h y s iol og ic b r e ed i n g

season, and i t must be differentiated from the syn-

drome of mares with silent heat. In addition, mares

t h a t h a v e b e e n b r e d a n d d o n o t r e t u r n t o h e a t a n d

are later diagnosed as not pregnant may also have a

persistent corpus luteum.Diagnosis of a persistent corpus luteum is made by

an analysis of plasma progesterone concentrations

or a clinical response to pr ostaglandin a dministra-

tion. Progesterone concentra tions 1.0 ng/ml are

indicative of th e presence of luteal activity. Mares

with a persistent corpus luteum will have good tone

in th e cervix an d ut erus on pa lpation, and th e cervix

w ill a p pe a r t ig h t a n d d r y on va gi n al s pe cu lu m

examination because of the influence of progesterone.

A persistent corpus luteum will usually be elimi-

n a t ed b y t h e a d m in is t r a tion of a s in gle in t r a -Fi g. 11. Mare wi t h ECD.

MARE SESSION






muscular dose of prostaglandins (PGF 2, 1 0 m g ;cloprostenol, 250 mg).

2. Anovulatory Follicles

Ovulation failure is a normal physiologic event forthe mare during the spring and fall transition periods.The development of anovulatory follicles may occa-

s i on a l l y occu r d u r i n g t h e p h y s i ol og ic b r e e d in gseason.1 Anovulatory follicles may be quite large(5–15 cm in diameter), persist for up to 2 months,a n d r e s u l t i n a b n o r m a l e s t r o u s b e h a v i o r a n d p r o -longed int erovulat ory intervals.11 The cau se of ovu-lation failure has been suggested to be endocrine inn a t u r e , e it h e r fr om a l a ck of s u ffi ci en t p it u i t a r ygonadotropin stimulation to induce ovulation orfrom insufficient estrogen production from th e fol-licle it self.

Anovulatory follicles may contain blood and areconsequently often termed hemorrhagic follicles.The hemorrhage can be detected ultrasonically asscattered free-floating echogenic spots within the

fol li cu l a r fl u id . T h e fol li cu l a r fl u id m a y for m agelatinous, hemorrhagic mass within the follicularlumen (Fig. 12). Ultra sonograph ically, these stru c-tures may contain echogenic fibrous ban ds travers-ing the follicular lumen (Fig. 13). A thickening of the follicular wall may be observed in some anovula-tory follicles. This t hickening ma y be associatedwith luteinization of the follicular wall. In somemares, plasma progesterone concentrations may beelevated over baseline levels because of the presenceof luteal t issue. The administration of prostaglan-dins may result in the destruction of the luteal cellsin those mares.

A majority of the anovulatory follicles will sponta-

n e ou s ly r e g r e ss i n 1 – 4 w e e k s. H u m a n ch or i on i cgona dotropin (2500 IU IV) or Gn RH (2.2 mg SQ) ma yinduce ovulat ion or lut einizat ion of some persistentanovulatory follicles. Unfortu na tely, most persis-tent follicles are not affected by huma n chorionicgonadotropin or GnRH treatment.

Pregnancy does not usually occur if a persistentfollicle eventually spontaneously ovulates or is in-

duced to ovulat e. This is likely a result of degenera-tion of the oocyte over t ime. Pr egnancy obviouslywill not occur if the follicle becomes hemorrhagic orluteinized with out ovulat ing.

4. Discussion

A majority of ovarian abnormalities can be diag-nosed with a minimum of equipment or diagnostictests. However, some abnorma lities require a moree xt e n s i ve e va l u a t i on , w h i ch m a y i n cl u d e b loodsamples for hormone an alysis or kar yotyping.

Disorders such as persistent an ovulat ory follicles,p e r si st e n t cor p or a l u t ea , a n d ov a r ia n h e m a t om a s

usually will resolve spontaneously over time if treat-ment is not administered. Surgical intervention isw a r r a n t e d f o r o v a r i a n t u m o r s t h a t h a v e p o t e n t i a leffects on the contra lateral ovary, cause recurrentabdominal pain, or have potent ial for metast asis.

A decision to remove one or both ovaries should bem a d e on l y a f t er ca r e fu l d e li be r a t ion . I f a cl ea rdiagnosis cann ot be determined on clinical signs,palpation, ultrasonography, hormone analysis, oroth er diagnostic tests, it ma y be prudent to postpones u r g e r y u n t i l i t i s c e r t a i n t h a t t h e o v a r y w i l l n o tretu rn t o normal function.Fig. 12. Persistent a novulatory follicle.

Fig. 13. Sonograph of a persistent an ovulatory follicle.

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ovarian tumour mare

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