TENOSYNOVITIS OF THE DEEP DIGITAL FLEXOR TENDON IN HORSES

R. W. Van Pelt, W. F. Riley, Jr. and P. J. Tillotson*

INTRODUCTION

TENOSYNOVITIS of the deep digital flexor ten-don (thoroughpin) in horses is manifested bydistention of its tarsal synovial sheath due toformation of an excessive synovial effusion. Un-less tenosynovitis is acute, signs of inflamma-tion, pain or lameness are absent (1). Tendinitiscan and does occur in conjunction with inflam-mation of the tarsal synovial sheath.As tendons function they are frequently sub-

jected to considerable strain, peritendinouspressure, and friction between the parietal andvisceral layers of the tendon sheath (2). Acutedirect trauma or trauma that is multiple andminor can precipitate tenosynovitis. In acutetenosynovitis of the deep digital flexor tendon,the ensuing inflammatory reaction affects thetarsal synovial sheath, which responds to in-flammation by formation of an excessive syno-vial effusion. Chronic tenosynovitis follows theacute form or it can be insidious in onset. Itis characterized by persistent synovial effusions,stenosis of the tendon sheath, or adhesions be-tween the parietal and visceral layers of thetendon sheath and the enveloped tendon (6,8). Riziform bodies may be present in synovialeffusions in chronic tenosynovitis.

Therapy in this group of horses was directedat preventing formation of excessive synovialeffusion by aspiration of the tarsal synovialsheath and the intrathecal injection of anadrenocortical steroid or one of its syntheticanalogues. Presented in this report are clinicalsigns, response to intrathecal injection of syn-thetic steroids, and results of synovial effusionanalyses. Analyses of synovial effusions wereperformed to characterize synovial effusionsproduced in horses affected with tenosynovitisof the deep digital flexor tendon.

MATERIALS AND METHODS

The tarsal synovial sheaths of the deep digi-tal flexor tendon in eight clinically affectedhorses were aspirated and injected with syn-thetic steroids at the time of diagnostic aspira-tion (Table I). Since synovial fluid wasunobtainable from normal synovial tendon

'Department of Pathology (Van Pelt) and De-partment of Large Animal Surgery and Medicine(Riley and Tillotson), College of Veterinary Medi-cine, Michigan State University, East Lansing,Mich. 48823.

sheaths, statistical comparisons were made be-tween certain values determined for synovialeffusions from tarsal synovial sheaths ofaffected horses and synovial fluids from thetibiotarsal joints of control horses.

Control HorsesFive healthy horses ranging in age from

four to nine years were used as controls. Fourof the horses were Thoroughbreds and onehorse was of Quarter Horse breeding. Allcontrol horses were geldings. Synovial fluidsamples were obtained from the tibiotarsal joint.

Hematologic DeterminationsBlood samples for determination of serum

sugar content (measured as total reducing sub-stances) were obtained from the jugular veinprior to aspiration of the tarsal synovial sheathin affected horses and the tibiotarsal joint incontrol horses. The clot was allowed to retractat 50 C and the samples were then centrifugedat 1,600 g at 50 C.

Synovial Effusion DeterminationsSynovial effusion samples were transferred

from aspirating syringes to screw-capped tubeswhich contained dried dipotassium ethylene-diaminetetraacetatel (EDTA) in a ratio of 2mg of EDTA per milliliter of synovial effusion.Synovial fluid samples from the tibiotarsaljoints of control horses were not transferred totubes containing EDTA. Tests for relativeviscosity (RV), mucinous precipitate quality,total protein content, albumin: globulin (A:G)ratio, and sugar content (measured as totalreducing substances) were performed on syno-vial effusions and synovial fluids after centri-fugation at 1,600 g at 50 C (5, 12, 15, 18).Total erythrocytic and leukocytic counts weredetermined from noncentrifuged portions ofthe synovial effusion and synovial fluid samples(12). Smears for differential counts werestained with Wright's stain. One hundredleukocytes were identified and counted (neu-trophils, lymphocytes, monocytes, macro-phages, and eosinophils).

Bacteriologic DeterminationsA portion of the synovial effusion sample

from two of the horses was transferred to a

ICambridge Chemical Products, Inc., Dearborn,Mich.

35

CAN. VET. JOUR., Vol. 10, no. 9, September, 1969

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236

TENOSYNOVITIS

sterilized test tube immediately following aspi-ration of the tarsal synovial sheath. Synovialeffusion samples were inoculated into brainheart infusion2 semisolid (0.15% agar) andbovine blood agar plates, and incubated at 370C. Negative cultures were held up to 10 days.

RESULTS

Clinical SignsTenosynovitis of the deep digital flexor ten-

dol was unilateFal in all horses and was mani-fesd by a fluctuant, palpable distention of itstarsal synovial sheath. The tarsal synovialsheath was distended on both medial andlateral sides of the tarsus; however, the great-est degree of distention was limited to themedial aspect of the tarsus. Degree of disten-tion was variable, dependent on the capacityof individual tarsal synovial sheaths for reten-tion of excessive synovial effusion. Tenosyno-vitis was chronic in all horses at the time ofclinical examination, and signs of inflammation,as manifested by heat and pain on palpation,and lameness were not apparent. None of thehorses had developed adhesions between theparietal and visceral layer. of the tarsal synovialsheath, and the tendon of the deep digital flexor.

Clinical Response to Intrathecal InjectionAspiration of affected tarsal synovial sheaths

provided symptomatic relief from intrathecalpressure and had a therapeutic effect by re-moving excessive synovial effusion. Intrathecalinjection of synthetic steroids controlled forma-tion of excessive synovial effusions in tarsalsynovial sheaths. Dosage and choice of inject-able synthetic steroid in each horse was deter-mined by the degree of distention of the tarsalsynovial sheath and the approximate durationof the synovial effusion (Table I). Acute in-flammation was not a factor in determiningtherapeutic dosages of synthetic steroids in thisgroup of horses.

Response to intrathecal injection of varioussynthetic steroids was manifested clinically byresolution of excessive synovial effusion and aconcomitant reduction in distention of theaffected tarsal synovial sheath. Clinically,favorable response to the intrathecal injectionof synthetic steroids generally required fromthree to six weeks. Despite intrathecal injectionof synthetic steroids, a minor palpable periten-dinous fibrosis persisted to some degree in themore chronically affected tarsal synovialsheaths. Advanced peritendinous fibrosis madeit difficult to achieve complete reduction of

2Difco Laboratories, Inc., Detroit, Mich.

chronically affected tarsal synovial sheaths.When possible, the affected tarsal synovialsheath was kept under a pressure bandageuntil resolution of excessive synovial effusionwas achieved.

Five tarsal synovial sheaths were injectedwith 6 a-methylprednisolone acetate3 (40 mg /cc) and two tarsal synovial sheaths receivedinjections of 6 a-methyl, 17 a-hydroxyproges-terone acetate4 (50 mg / cc). Excessive syno-vial effusion was controlled in a three-year-oldStandardbred gelding (Table I, horse 8)affected with chronic tenosynovitis of the tarsalsynovial sheath following the second intrathe-cal injection of 30 mg of 9-fluoroprednisoloneacetate5 (2 mg / cc) and 300 mg of 6 a-methyl,17 a-hydroxyprogesterone acetate.

Intrathecal injection of 6 a-methyl, 17 a-hydroxyprogesterone acetate did not alter theestrous cycle of one mare or impair fertility inone stallion (Table I, horses 6 and 7).

Synovial Effusion FindingsAll synovial effusions from horses affected

with tenosynovitis of the deep digital flexortendon were transudative. Quantity and grossappearance of synovial effusions were recordedat the time of aspiration and intrathecal injec-tion (Table II). Potential capacity of indivi-dual tarsal synovial sheaths and the durationof tenosynovitis determined the quantity ofretained excessive synovial effusion. Grossly,synovial effusions were either pale yellow andclear, or amber and clear, or amber andopaque in appearance. One synovial effusioncontained some flocculent material. Synovialxanthochromia was more pronounced in ambersynovial effusions due to continued intrathecalhemorrhage and subsequent hemolysis ante-cedent to aspiration.

Relative viscosity and mucinous precipitatequality were determined for each synovialeffusion sample (Table III). These proceduresdetermined the relative viscosity of synovialeffusions and, qualitatively the concentrationand polymerization of the hyaluronic acidmoiety in synovial effusions from horsesaffected with tenosynovitis of the deep digitalflexor tendon. There was no significant (P >0.05) difference between the relative viscosityof synovial effusions from the tarsal synovialsheaths of affected horses (RV = 2.44) andsynovial fluids from the tibiotarsal joints ofcontrol horses (RV = 3.72). Mucinous preci-

3Depo-Medrol, Upjohn Company, Kalamazoo,Mich.

4Depo-Provera, Upjohn Company, Kalamazoo,Mich.

5Predef 2X, Upjohn Company, Kalamazoo, Mich.

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TABLE IIGROSS APPEARANCE AND QUANTITY OF SYNOVIAL EFFUSIONS

Affected Quantitytarsal (ml/tarsal

Horse synovial Gross synovialNo. sheath appearance sheath)

1 Right Pale yellow, 140.0clear

2 Left Amber-opaque 50.03 Left Amber-clear 30.04 Left Pale yellow, 110.0

clear5 Right Amber-opaque, 10.0

some flocculentmaterial

6 Left Amber-opaque 24.07 Right Pale yellow, 70.0

clear8 Left Pale yellow, 250.0

clearMean 85.5S.E. 27.9

S.E. = Standard error of the mean.

TABLE IIIRELATIVE VISOCITY, MUCINOUS PRECIPITATE QUALITY,

TOTAL PROTEIN CONTENT, AND ALBUMIN:GLOBULIN RATIO OF SYNOVIAL EFFUSIONS

Relative Mucinous Total Albumin:Horse viscosity precipitate protein globulinNo. (at 37 °C) quality* (Gm/100 ml) ratio

Affectedhorses

1 1.32 Fair ....

2 1.57 Fair .... ....

3 2.54 Poor .... ....

4 2.07 Fair 1.25 7.335 2.16 Very poor 4.00 1.866 6.47 Very poor 2.29 1.067 1.81 Poor 1.70 0.838 1.59 Poor 2.73 2.21

Mean 2.44 2.39 2.66S.E. 0.59 0.47 1.20

Controlhorses

1 3.55 Normal 1.04 5.502 3.91 Normal 1.57 0.313 2.61 Normal 1.39 1.624 4.54 Normal 1.54 8.065 3.97 Normal 1.37 1.58

Mean 3.72 1.38 3.41S.E. 0.32 0.10 1.45

S.E. = Standard error of the mean.*Mucinous precipitate quality: normal = tight, ropy clump in a

clear solution; fair = soft mass in a slightly turlbid, xanthochromic, oramber solution; poor = small, friable masses in a turbid, xantho-chromic, or amber solution; and very poor = few flecks in a veryturbid, xanthochromic, or amber solution of 7 N glacial acetic acid(2.5%).

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pitate quality ranged from fair (soft mass in a

slightly turbid, xanthochromic, or amber solu-tion) to very poor (few flecks in a very turbid,xanthochromic, or amber solution) for synovialeffusions from affected tarsal synovial sheaths.All synovial fluid samples from the tibiotarsaljoints of control horses were normal (tight,ropy clump in a clear solution). Decreasedconcentration and loss of polymerization in thehyaluronic acid moiety in most synovial effu-sions was denoted by formation of small, fri-able precipitates when 1 ml of synovial effusionwas added to 4 ml of a 2.5% aqueous solutionof 7 N glacial acetic acid (12).

Results of total protein determinations andA:G ratios partially confirmed the transudativeproperties of synovial effusions (Table III).The mean total protein content in synovialfluid from control horses (1.38 Gm/100 ml)was slightly less than in synovial effusionsfrom affected horses (2.39 Gm/100 ml). Themean A:G ratio (3.41) was slightly higher insynovial fluid from control horses than themean A:G ratio (2.66) in synovial effusionfrom horses affected with tenosynovitis of thedeep digital flexor tendon.Serum and synovial effusion sugar content

(measured as total reducing substances) were

determined simultaneously (Table IV). Thesugar content in synovial effusions ranged from97 mg/100 ml less than serum sugar content to18 mg/100 ml greater than serum sugar con-tent. The mean synovial effusion sugar contentin affected horses was 40 mg/100 ml less thantheir mean serum sugar content. Mean synovialeffusion sugar content in horses affected withtenosynovitis of the deep digital flexor tendonwas 29% less than their mean serum sugarcontent. This difference was significant (P <0.05). The mean sugar content in synowvialeffusion from tarsal synovial sheaths was sig-nificantly (P < 0.05) less than in synovialfluid from tibiotarsal joints. The sugar contentin synovial fluid from tibiotarsal joints of con-trol horses ranged from 32 mg/100 ml lessthan sugar content in serum to 12 mg/100 mlgreater than sugar content in serum. Therewas a mean synovial fluid sugar difference forcontrol horses of 9 mg/100 ml less than theirmean serum sugar content. Mean synovial fluidsugar content in control horses was 4% less thantheir mean serum sugar content, which was notsignificant (P > 0.10). These differences insugar content established a serum:synovialeffusion sugar ratio of 1.4:1 for horses affectedwith tenosynovitis of the deep digital flexor

TABLE IVCOMPARISON OF SERUM AND

SYNOVIAL EFFUSION SUGAR CONTENT

Serum Synovial Serum: synovialHorse sugar sugar sugar differenceNo. (mg/100 ml) (mg/100 ml) (mg/100 ml)*

Affectedhorses

1 218 162 <562 100 105 > 53 105 32 <734 109 57 <52

[i ... 121 ....64 82 > 18

7 94 69 <258 171 74 <97

Mean 123 88** <40S.E. 20 14 16

Controlhorses

1 99 67 <322 103 105 > 23 65 69 > 44 107 100 < 75 138 150 > 12

Mean 102 98 < 9S.E. 12 15 6

S.E. = Standard error of the mean. *Synovial sugarcontent less than or greater than the simultaneouslydetermined serum content. **Significantly (P < 0.05)less than corresponding serum sugar content.

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tendon. Serum:synovial fluid sugar ratio forcontrol horses was 1:1.

Total erythrocytic counts ranged markedlyfrom one synovial effusion to another (TableV). There was a close relationship betweengross appearance of the synovial effusion andthe total erythrocyte count (i.e., the highesterythrocytic counts were in amber and clearor amber and opaque synovial effusions). Noerythrocytes were present in synovial fluidfrom the tibiotarsal joints of control horses.Total leukocytic counts did not vary as mark-edly as total erythrocytic counts (Table V).Leukocytic counts for synovial fluid from con-trol horses were low. Increased relative num-bers of neutrophils were associated withincreased numbers of erythrocytes. Numerouslaked erythrocytes were noted on synovial effu-sion smears. Many degenerated leukocytes anda few synovial intimal cells were noted, butexcluded from both total and differential leuko-cytic counts.

Bacteriologic FindingsThe two synovial effusion samples submitted

for bacteriologic studies were negative on cul-ture (Table I, horses 5 and 8).

DIsCUSSION

Tenosynovitis of the deep digital flexor ten-don in horses was manifested by marked dis-tention of its tarsal synovial sheath due toformation and retention of an excessive transu-dative synovial effusion. Distention of thetarsal synovial sheath of the deep digital flexor

tendon can be confused with tarsal hydrarth-rosis (bog spavin) when the medioplantar andlateroplantar pouches of the tibiotarsal syno-vial sac are visibly distended (1, 6, 16). Dis-tention of the tarsal synovial sheath is generallygreatest on the medial aspect of the tarsus. Incontrast to the location of the medioplantarpouch of the tibiotarsal synovial sac, the tarsalsynovial sheath of the deep digital flexor ten-don extends 5 to 7 cm proximal to the medialmalleolus of the tibia and 5 to 7 cm distal tothe proximal end of the third metatarsal bone(10). Inflammation of the large bursa inter-posed between the gastrocnemius and super-ficial digital flexor tendons (intertendinouscalcaneal bursitis) can also present a problemin differential diagnosis (17).The pathogenesis of tenosynovitis of the

deep digital flexor tendon wherein excessivetransudative synovial effusions are formed andpersist in its tarsal synovial sheath is a poorlyunderstood syndrome in the horse (1, 6, 8).Inflammation of the tendon of the deep digitalflexor can and does occur in conjunction withinflammation of its tarsal synovial sheath.Acute tenosynovitis can be caused by tendonstrain, friction between the parietal and vis-ceral layers of the tarsal synovial sheath, peri-tendinous pressure, and acute direct trauma tothe tendon of the deep digital flexor and itstarsal synovial sheath (2). Acute tenosynovitisof the deep digital flexor tendon is manifestedby rapid filling of the tarsal synovial sheath,heat, pain, and lameness (1). Acquired hyper-sensitivity to an unknown foreign agent oragents can precipitate acute tenosynovitis (8).

TABLE VCYTOLOGIC PROPERTIES OF SYNOVIAL EFFUSIONS

Neutro- Lympho- Mono- Macro- EosinoHorse Erythrocytes Leukocytes phils cytes cytes phages philsNo. (per cmm) (per cmm) (%) (%) (%) (%) (%)

Affected horses1 0 175 7 73 13 7 02 8,000 500 30 20 50 0 03 3,000 600 52 1 44 1 24 0 44 3 85 12 0 05 20,500 367 61 27 12 0 06 21,500 200 8 65 22 1 47 111 311 0 95 5 0 08 1,975 511 5 93 2 0 0

Mean 6,886 339 20.8 57.4 20.0 1.1 0.8

Control horses1 0 44 0 30 64 6 02 0 144 2 52 40 6 03 0 78 4 64 26 6 04 0 78 0 82 18 0 05 0 67 0 66 31 0 3

Mean 0 82 1.2 58.8 35.8 3.6 0.6

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Chronic tenosynovitis may follow the acutecondition or develop from trauma that is mul-tiple and minor. It is possible that repeatedsubclinical strain of the tendon of the deepdigital flexor or inapparent trauma could de-velop into chronic tenosynovitis. Chronic teno-synovitis is manifested by a fluctuant distentionof the tarsal synovial sheath due to continuedformation and retention of an excessive syno-vial effusion. Fibrosis of the parietal layer ofthe tarsal synovial sheath further enhanceschronicity. Tenosynovitis of the deep digitalflexor tendon can develop in an insidiousmanner (8). Horses in this investigation devel-oped an insidious form of tenosynovitis withoutsigns of inflammation. In the absence of anaccurate history, it proved impossible to dis-tinguish between chronic tenosynovitis and theinsidious form of tensynovitis. A low degree oftarsal joint angulation (i.e. too straight in thetarsal joint) can predispose horses to tenosyno-vitis of the deep digital flexor tendon (9).

Aspiration of synovial effusions and intrathe-cal injection of synthetic steroids provided apalliative means of effectively controlling pro-duction and retention of excessive synovialeffusions, and reducing fibrosis in tarsal syno-vial sheaths. The mechanism is unknownwhereby adrenocortical steroids or their syn-thetic analogues suppress formation and re-tention of excessive transudative synovialeffusions (13, 14). Adrenocortical steroids sup-press inflammation without regard to etiologyor type (i.e. suppurative or nonsuppurative)(2, 11). Chronic tenosynovitis or the insidiousform of tenosynovitis did not respond rapidlyto the intrathecal action of synthetic steroids.Intrathecal injection of 6 a-methyl, 17 a-hydroxyprogesterone acetate suppressed for-mation of synovial effusions and revealed aprolonged duration of action when comparedto 6 a-methylprednisolone acetate. These datareflected either an intrathecal depot effect of6 a-methyl, 17 a-hydroxyprogesterone acetateor a delayed rate of tissue inactivation. Theaddition of 9-fluoroprednisolone acetate to 6a-methyl, 17 a-hydroxyprogesterone acetatein a 1:10 ratio hastened this antitransudativeeffect without interfering with its prolongedduration of activity. These results indicatedthat 6 a-methyl, 17 a-hydroxyprogesteroneacetate possesses features characteristic of 11p-hydroxylated, C21 acetate steroids (3, 4).Addition of the 6 a-methyl group to the pro-gesterone molecule enhances its biologic acti-vity. Apparently oxygen functions at C-ll,C-17, and C-21 are not obligatory for adreno-cortical steroid activity (4).

Tenosynovitis implies inflammation of the

synovial membrane lining the tarsal synovialsheath as opposed to its fibrous outer layer;however, the fibrous layer is usually affected(6). Inflammation is not a prerequisite for for-mation and retention of excessive transudativesynovial effusions in tarsal synovial sheaths(8). Synovial effusions from all eight horses inthis investigation were chronic at the time ofaspiration; however, these synovial effusionsreflected no inflammatory changes in the syno-vial membranes lining these tarsal synovialsheaths. Chronic tenosynovitis and insidiousforms of tenosynovitis of the deep digital flexortendon were indistinguishable, both clinicallyand by synovial effusion analyses. The primarydifference between the two forms of tenosyno-vitis being one of etiology, viz. chronic teno-synovitis of the deep digital flexor tendonfollowed the acute form of tenosynovitis,whereas the insidious form of tenosynovitis de-veloped without a history or signs of previousinjury or inflammation. Both forms of tenosyno-vitis were characterized by retention of self-perpetuating transudative synovial effusions.Pathologic changes in synovial effusions ofchronic tenosynovitis were similar to those intarsal hydrarthrosis in horses, wherein excessivetransudative synovial effusions develop andpersist (16).

Analysis of synovial effusions and interpre-tation of findings can provide an excellentmeans of differentiating between acute andchronic forms of tenosynovitis (11). If infec-tion is suspected, bacteriologic cultures of thesynovial effusion should be performed. Sincelittle information is available on normal syno-vial fluid from tendon sheaths, it must beassumed that it is analogous to the synovialfluid of diarthrodial joints. Pathologic changesin joint diseases may therefore have a corollaryin tenosynovitis. Synovial xanthochromia wasmost pronounced in amber synovial effusionsdue to continued intrathecal hemorrhage andsubsequent hemolysis. Grossly, pale yellowsynovial effusions from tarsal synovial sheathsmost closely resembled normal synovial fluidfrom the tibiotarsal joints of control horses.

Relative viscosity of synovial effusions (RV= 2.44) from tarsal synovial sheaths was lowerthan the relative viscosity of synovial fluid(RV = 3.72) from the tibiotarsal joints of con-trol horses. Despite fair, poor, or very poormucinous precipitates (indicative of reducedhyaluronic acid concentration and polymeriza-tion), synovial effusions maintained sufficientviscousness to ameliorate the deleterious effectsof friction within tarsal synovial sheaths. High-ly polymerized hyaluronic acid in synovial fluidis not necessary for normal joint or tendon

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sheath lubrication (7). The proteins of bloodhave no lubricating properties; however, a pro-tein moiety forms an intrinsic component ofthe hyaluronic acid-protein complex. This pro-tein moiety may serve as a prosthetic group foradsorption of mucin onto a moving surface(i.e. the articular cartilages or synovial mem-branes lining bursas and tendon sheaths). Ad-sorption of hyaluronic acid to synovial intimalcells lining tendon sheaths forms an essentialprerequisite for boundary lubrication.

Serum:synovial effusion sugar ratio was1.4:1 in affected horses, compared to the 1:1serum:synovial fluid ratio in control horses.Sugar levels in synovial effusions suggest thatthe equilibrium between a bursa and blooddiffers in comparison to the sugar equilibriumregulated by the blood-joint barrier (11). Lowsugar levels in the absence of bacteria ormarked leukocytosis are unusual in nonsuppu-rative synovial effusions in joints. The rate ofsugar utilization by tendon sheaths and bursasapparently differs from that of joints. Articularcartilages in diarthrodial joints may requirehigher levels of readily available sugar in thesynovial fluid.

Erythrocytic and leukocytic counts in syno-vial effusions from horses affected with teno-synovitis of the deep digital flexor tendon wereincreased in comparison to erythrocytic andleukocytic counts in synovial fluid from thetibiotarsal joints of control horses. Amber syno-vial effusions had the highest erythrocytic andleukocytic counts. Increased numbers of leuko-cytes either gained entrance to the tarsal syno-vial sheath when hemorrhage occurred ormigrated into tendon sheaths in response toirritation arising from the products of ery-throcytic destruction (i.e. bilirubin and hemo-siderin) (11).

SUMMARY AND CONCLUSIONS

Tenosynovitis of the deep digital flexor ten-don was manifested by distention of its tarsalsynovial sheath due to formation and retentionof an excessive transudative synovial effusion.Tenosynovitis of the deep digital flexor tendonwas chronic at the time of clinical examination.Tendon strain, peritendinous pressure, trauma,and intrathecal friction were considered pre-disposing causes. Absent were signs of inflam-mation, as manifested by heat and pain, andlameness. The cause of an insidious form oftenosynovitis of the tarsal synovial sheath ofthe deep digital flexor tendon was undeter-mined. Synovial effusions were analyzed fortheir physical, biochemical, and cytologic prop-

erties. Pathologic changes in synovial effu-sions were minor.

Therapeutic benefit was derived from aspira-tion of all available synovial effusion. Intra-thecal injection of 6 a-methylprednisoloneacetate and 6 a-methyl, 17 a-hydroxyproges-terone acetate provided a palliative means ofsuppressing formation and retention of exces-sive effusions. Results indicated that 6 a-methyl, 17 a-hydroxyprogesterone acetate hada prolonged duration of antitransudative activ-ity and possessed features characteristic of 11,/-hydroxylated, C21 acetate steroids. Clinicalresponse to intrathecal injection of syntheticsteroids was manifested by resolution of exces-sive synovial effusion and concomitant reduc-tion in distention of tarsal synovial sheaths. Apalpable peritendinous fibrosis persisted tosome degree in all horses.

RESUME

Une inflammation de la synoviale du flechis-seur profond des phalanges s'est manifesteepar une distention de la gaine tarsienne causeepar l'accumulation de synovie. Au moment del'examen clinique, l'inflammation etait chro-nique. On considerait comme causes predis-posantes les efforts et les pressions sur letendon, ainsi que les trauma et les frictions 'al'interieur de la gaine tendineuse. On n'a ob-serve aucun signe d'inflammation tel que lachaleur, la douleur ou une boiterie. La causede l'affection n'a pas ete determinee. Uneanalyse physique, biochimique et cytologiquedu liquide synovial n'a revele que des change-ments pathologiques mineurs.

L'aspiration de tout le liquide synovial pos-sible a apporte une certaine amelioration. Onpallia a la surproduction de synovie en injec-tant dans la gaine affectee de l'acetate de6-x-methylprednisolone et de l'acetate de 6-x-methyl, 17-x-hydroxyprogesterone. Les resul-tats prouverent que cette derniere substance aune action prolong6e sur la secretion de lasynovie et, en outre, qu'elle possede des carac-teristiques des ac6tates C21 de steroides, 11-B-hydroxyle's. L'injection de steroides de syn-these provoqua la disparition de l'exces desynovie et, consequemment, une diminution dela distension de la gaine tarsienne. Une fibroseperitendineuse, decelable a la palpation, per-sista chez tous les chevaux.

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11. ROPES, M. W. and W. BAUER. Synovial FluidChanges in Joint Diseases. Cambridge, Mass:Harvard University Press. 1953.

12. VAN PELT, R. W. Properties of Equine Syno-vial Fluid. J. Am. vet. med. Ass. 141: 1051.1962.

13. VAN PELT, R. W. and W. F. RILEY, JR. Thera-peutic Management of Tarsal Hydrarthrosis(Bog Spavin) in the Horse by Intra-ArticularInjection of Prednisolone. J. Am. vet. med.Ass. 151: 328. 1967.

14. VAN PELT, R. W. Intra-Articular Injection of6 a-Methyl, 17 a-Hydroxyprogesterone Ace-tate in Tarsal Hydrarthrosis (Bog Spavin) inthe Horse. J. Am. vet. med. Ass. 151: 1159.1967.

15. VAN PELT, R. W. Characteristics of NormalEquine Tarsal Synovial Fluid. Can. J. comp.Med. 31: 342. 1967.

16. VAN PELT, R. W. Tarsal Hydrarthrosis (BogSpavin) in the Horse: Blood, Serum, andSynovial Fluid Findings. Am. J. vet. Res.29: 569. 1968.

17. VAN PELT, R. W. and W. F. RILEY, JR. Trau-matic Subcutaneous Calcaneal Bursitis (Cap-ped Hock) in the Horse. J. Am. vet. med.Ass. 153: 1176. 1968.

18. WEICHSELBAUM, T. E. An Accurate andRapid Method for the Determination of Pro-teins in Small Amounts of Blood, Serum, andPlasma. Am. J. cin. Path. 16: 40. 1946.

BOOK REVIEW

Animal Agents and Vectors of Human Disease.Third Edition. E. C. Faust, P. C. Beaver andR. C. Jung. Published by Lea & Febiger,Philadelphia and the Macmillan Company ofCanada, Toronto. 1968. 461 pages. Price$12.50.

This is the newly revised edition of an estab-lished text written principally for medical andpublic health workers. Although it is not a textbook of veterinary parasitology, it does holdsome interest for workers in the field of veter-inary epidemiology. It is a rather comprehen-sive volume, covering general principles ofparasitology followed by sections on Protozoa,Hehninths and Arthropods. A further section,headed "Technical Aids" covers proceduresuseful in the diagnosis of parasitic diseases.Full author and subject indices are included.

As would be expected from a revised edition,there are few typographical errors. The spell-ing of "species" on page 322 happens to be onenoted. The illustrations are generally excellent,including the grouped set of color plates ofamoebae and Plasmodium spp. One or twodrawings are less useful, for example, a linedrawing of a larval ascarid on page 232.Of the various sections, it is felt that Section

IV (Arthropods as Agents and Vectors) mightbe rearranged slightly to arrive at a moresystematic subdivision of headings. In this samesection there are one or two common names ofinsects given which differ from those usuallyattached to the species.

These, however, are very minor items, andthe book remains a most useful volume whichserves as an excellent reference in the field ofhuman parasitology. D. P. Gray.

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