Veterinary Surgery, 19,5,392-397, 1990

Equine Post-anesthetic Lameness

A Retrospective Study

MEGHAN T. RICHEY, DVM, MELISSA S . HOLLAND, DVM, DiplomateACVA,

CHARLES J. M C G R A T H , DVM, DiplomateACVA, NICHOLAS H. DODMAN, BVMS, MRCVS, DVA, DiplomateACVA,
DURWOOD B. MARSHALL, BS, MICHAEL H. COURT, B V ~ C DiplomateACVA,
, WENDY M. NORMAN, Bvsc,
and DAVID c. SEELER, DVM, MSc, DiplomateACVA

The incidence of post-anestheticlameness in 655 horses undergoing 733 anesthetic episodes

over a 3 year period was 6.4%. Nineteen factors previously reported or proposed to play a
role in the development of post-anesthetic lameness were evaluated statistically. Only hypo-
tension and the duration of the anesthetic period were significant factors.

Imaybeisoccur
T WELL KNOWN that general anesthesia in horses can
complicated by post-anesthetic lameness, which
in the form of myopathy or neuropathy.’-’6
Depending on the severity of the lameness, associated
problems range from an increase in total recumbency
tirne to death.10.14.~h.?6
Until 1973, post-anesthetic lameness was thought to
be a neuropathic condition.’-4 While most cases now ap-
season of the year. body position during recumbency,
duration of anesthesia, type of procedure, and the physi-
ologic factors of acid-base status, circulatory status, and
body temperature. Attempts also have been made to link
post-anesthetic lameness with malignant hyperthermia
and exercise induced myopathy because these syn-
dromes frequently resemble each other ~ l i n i c a l l y . ‘ ~ ~ ~ ~ ~ -
‘5.’8.30 Although several metabolic alterations have been

pear to be of muscular origin, there is evidence that mus-
cles and nerves may be affected simultaneously. “)xm.27
Whatever the origin of postanesthetic lameness, the
damage to muscles or nerves usually is not recognized
until the recovery phase of anesthesia.’.’’.15.2’.24.26 S’ince
the cause of these syndromes has not yet been identifed,
prediction of their occurrence and their treatment have
been largely unrewarding.‘,”’ It is difficult to replicate the
clinical course of post-anesthetic lameness without pro-
longed recumbency on nonpadded surfaces, hypoten-
sion, intentional poor positioning, or compression of the
axillary artery.l.6.10.17.20.22.28
I n the last 15 years, investigators have proposed many
theories regarding the cause of postanesthetic lame-
ness.l.h.10.11.13-18.’3.~ ”.2h,29 Contributing factors have been
grouped into intrinsic and extrinsic or management fac-
tors.’ Intrinsic factors include the age, breed, weight, and
sex of the horse as well as its degree of fitness at the time
of anesthesia. Extrinsic and management factors include
implicated, the most commonly proposed causes include
prolonged recumbency, hypotension, and localized mus-
cular i s c h e m i a . ’ . 6 . ? . Y . ~ ~ . ~ ~ - ~ X . 2 ~ . 2 4 - 2 6 . ~ Y
Despite the development of general anesthetic tech-
niques designed to minimize alterations in cardiopulmo-
nary and neuromuscular function, the incidence of post-
anesthetic tameness in healthy horses continues at an un-
acceptable l e ~ e l . ~ . ~I .This
~ ~ . study
~ ~ . ’was undertaken to
identify factors that contribute to the development of
post-anesthetic lameness in light of current anesthetic
and surgical techniques.
Materials and Methods
Nineteen parameters previously reported or proposed
to contribute to post-anesthetic lameness were retrieved
from the records of 655 horses and ponies undergoing
733 general anesthetics at Tufts University School of
Veterinary Medicine from March I985 through March

From the Department of Surgery, Section of Anesthesia, School of Veterinary Medicine, Tufts University, North Grafton, Massachusetts
(Richey, Holland, Dodrnan,Court, Norman, Seeler), Virginia-MarylandRegional College of Veterinary Medicine, Virginia Tech, Blacksburg, Virginia
(McGrath), and Tufts Computer Services, Tufts University, Medford, Massachusetts (Marshall).
The authors thank Peter Pascoe, BVSc, and Robin Gleed, BVSc, for the original concept; and Katey Burrows Kintzer and Kathy Bombard,
the large animal anesthesia technicians, for their assistance in gathering these data.
Reprint requests: Charles J. McGrath. DVM, Virginia-MarylandRegional College of Veterinary Medicine, Virginia Tech, Blacksburg, VA 24061.

392
 RICHEY, HOLLAND, McGRATH, DODMAN, MARSHALL, COURT, NORMAN, AND SEELER 393

TABLE 1. Factors Analyzed for Potential Contribution cated that a horse was not any more lame than at induc-
to Post-Anesthetic Lameness tion or was lame only as a direct result of the surgical
Intrinsic: Breed
procedure. A barely perceptible lameness was defined as
Weight grade 1. A horse with a grade 5 lameness was in severe
Age pain or was recumbent. Transient knuckling at the fet-
Sex locks while attempting to stand successfully was not
Degree of fitness scored as a lameness. Any horse with a post-anesthetic
History of exercise induced myopathy
Extrinsic: Season of the year
lameness of grade 1 through 5 was categorized as
Administration of pre-anesthetic or intraoperative PAL( +). Horses with a grade 0 lameness were PAL( -).
medications The number of anesthetic episodes in which horses de-
Induction technique veloped post-anesthetic lameness was compared by chi-
Anesthetic maintenance square to the number in which they did not. The as-
Rate of intravenous fluid administration
Duration of anesthesia
Procedure performed TABLE 2. The Effect of Anesthetic Duration on the
Recumbent position Occurrence of Post-Anesthetic Lameness
Physiologic: Mean arterial pressure
PaO, Number of Anesthetics
PaCO,
PH, Accumulated
Raw Totals Totals
Duration of Percent
1988. Records from other horses that did not include all Anesthesia Not Lame Lame Not Lame Lame Lame
19 parameters were excluded from further study. (hr.) (A) (B) (C) (D) (0
Contributing factors were grouped as intrinsic, extrin-
0.00-0.25 7 0 686 0 0.0
sic (management), and physiologic (Table 1). The six in- 0.26-0.50 25 0 679 0 0.0
trinsic factors were breed, weight, age, sex, degree of fit- 0.51-0.75 23 0 654 0 0.0
ness, and prior history of exercise induced myopathy. 0.76-1 .OO 59 3 631 3 0.5
The degree of fitness was assessed as in training, in train- 1.01-1.25 38 1 572 4 0.7
ing but let down, not in training, or emergent with un- 1.26-1.50 100 1 534 5 0.9
known training status. Any prior history of exercise in- 1.51-1.75 54 2 434 7 1.6
duced myopathy was obtained from the owner or trainer, 1.76-2.00 109 7 380 14 3.5
or from hospital records. Extrinsic factors included the 2.01 -2.25 37 0 271 14 4.9
season ofthe year, drug administration before induction, 2.26-2.50 90 6 234 20 7.9
intraoperative drug administration. induction tech- 2.51-2.75 22 4 144 24 14.3
nique. anesthetic maintenance, rate of fluid administra- 2.76-3.00 58 13 122 37 23.3
tion. duration of anesthesia, type of procedure per- 3.01-3.25 16 1 64 38 37.3
formed, and recumbent position. Physiologic factors in- 3.26-3.50 12 3 48 41 46.1
cluded hypotension, hypoxemia, hypercarbia, and 3.51-3.75 11 1 36 42 53.8
3.76-4.00 10 3 25 45 64.3
acidemia.
Systemic blood pressure was recorded every 5 minutes 4.01 -4.25 1 0 15 45 75.0
and measured continuously through an arterial catheter 4.26-4.50 6 2 14 47 77.1
4.51-4.75 1 0 8 47 85.5
placed in the facial or metatarsal artery with the trans- 4.76-5.00 7
3 0 47 87.0
ducer or manometer zeroed at the point of the shoulder.
Hypotension was defined as a mean arterial pressure of 5.01-5.25 0 0 4 47 92.2
5.26-5.50 2 0 4 47 92.2
less than 70 mm Hg for 10 minutes or more. Hypoxemia, 5.51-5.75 0 0 2 47 95.9
hypercarbia, and acidemia were considered to be present 5.76-6.00 0 0 2 47 95.9
if at any time the PaO, was less than 100 m m Hg. the
6.01-6.25 0 0 2 47 95.9
PaC0, was more than 60 mm Hg, or the pH was less 6.26-6.50 1 0 2 47 95.9
than 7.35. 6.51-6.75 0 0 1 47 98.0
Horses were evaluated on a scale of 0 through 5 for the 6.76-7.00 1 0 1 47 98.0
appearance of lameness. Initial scoring of lameness was
done immediately after the horse stood in the recovery Accumulated totals were obtained for columns (C)and (D) by sum-
ming columns (A) bottom to top and (B) top to bottom, respectively. It
stall and efforts to ambulate became coordinated. Horses was assumed that a horse that was lame at any given anesthetic dura-
were examined at the walk by the anesthesiologist or sur- tion would also be lame after the next longer duration. Column (E) was
geon periodically over the next 2 hours. A grade o f 0 indi- calculated by dividing column (D) by the sum of columns (C) and (D).
394 EQUINE POST-ANESTHETIC LAMENESS

obtained by first subtracting the mean arterial pressure

(MAP) of each hypotensive horse (MAP < 70 mm Hg)
from 70. This resultant delta MAP value was multiplied
by the duration (in hours) of hypotension:
99
HI = (70 ~ MAP)

95
X Duration of Hypotension (hours) (1)
In each anesthetic record during the period of hypo-
tension, some variation in MAP was observed among the
80
(Y
5 minute intervals in which blood pressure recordings
were made. During initial data tabulation, these varia-
8 60
50
tions were minimized and simplified by using four hypo-
40 tensive ranges of 60-70, 50-70, 40-70, and 30-70 mm
Hg. For each of these four hypotensive ranges, the mid-
20 point value of MAP ( 6 5 , 6 0 , 5 5 , and 50, respectively) was
defined as the MAP and was used in the equation to de-
termine HI.
5
Ranges of HI values were defined (Table 3). The num-
ber of PAL( +) and PAL(-) horses was tabulated for each
I
HI range. The percentage of PAL horses for each HI was
calculated” (Table 3), and the HI response curve (Fig. 2)
was plotted.’* In the same manner as PAL/AD, PAL as
influenced by HI (PAL/HI) could be calculated. Since a
PAL incidence of 2% was considered acceptable, the
Duration of Anesthesia IHrs)
PAL/HI 2 was determined from the plotted data (Fig. 2).
Fig. 1. This probit plot of the percentage of lame horses in column
(E), Table 2, depicts the effect of anesthetic duration on development Results
of post-anesthetic lameness (PAL). From this graph (analogous to an
LDSodetermination), the PAL as influenced by anesthetic duration Post-anesthetic lameness occurred in 47 of 733 anes-
(PAL/AD) 50 would be 4 2 hours A more reasonably acceptable inci- thetic episodes (6.4%).None of the intrinsic factors had
dence of 2% PAL (PAL/AD 2) would likewise be determined as 1.6
hours TABLE 3. The Effect of Hypotension and Its Duration (Hypotension
Index) on Occurrence of Post-AnestheticLameness
~~

sumed level ofsignificance wasp < .05. To determine the Number of Anesthetics
level of contribution of each factor to the development Accumulated
of post-anesthetic lameness, the factors were grouped by Raw Totals Totalst
intrinsic. extrinsic, and physiologic classification for AN- Percent
OVA determination. The assumed level of significance Hypotension‘ Not Lame Lame Not Lame Lame Lame
wasp < .05. Index (HI) IAl fB\ (C) 0) (E)
Post-anesthetic lameness as influenced by the anes- 0.01-1.25 20 0 434 0 0.0
thetic duration (PAL/AD) was calculated in a manner 1.26-2.50 86 5 41 4 5 1.2
similar to that used for LDSodetermination.’’ In this 2.51-5 00 130 5 328 10 3.0
analysis, the anesthetic duration (time in hours) was sub- 5 01-10 00 125 11 198 21 9.6
stituted for the anesthetic “dose” (mg, %, etc). The num- 10.01-15 00 46 10 73 31 29.8
ber of PAL(+) and PAL(-) horses was counted and 15.01-20.00 12 4 27 35 56.5
summed for each 15 minute interval (Table 2). The re- 20.01-25 00 10 2 15 37 71.0
sultant anesthetic duration response curve (Fig. I ) was 25.01 -30.00 5 1 5 38 88.4
plotted as the duration in hours VJ. percent lameness 30.01-35 00 0 1 0 39 0.0
(probit).” The PAL rate we considered acceptable was
~

2%. Therefore, the PAL/AD 2, rather than PAL/AD 50 See text for calculation of the hypotension index
*

was determined from the plotted data (Fig. I).

To determine the effect hypotension and its duration
had on post-anesthetic lameness, the data were manipu-
lated to obtain a hypotension index (HI). The HI was
t Accumulated totals were obtained for columns (C) and (D) by
summing columns (A)bottom to top and (B) top to bottom, respectively.
It was assumed that a horse that was lame at a given HI would also
be lame after the next larger HI Column (E) was calculated by dividing
column (D) by the sum of columns (C) and (D)
 RICHEY, HOLLAND, McGRATH, DODMAN, MARSHALL, COURT, NORMAN, AND SEELER 395

TABLE 4. Breed Specific lncidence of Post-Anesthetic Lameness

99
Total PAL(-) PAL(+) PAL(+)
Breed No. No. No. %
95
Thorough bred 316 294 22 7.0
Standardbred 146 136 10 7.0
Quarter Horse 74 67 7 9.5
80
Arabian 59 56 3 1.7
Thorough bred X' 18 16 2 11.0
a 60 Warmbloodt 14 12 2 14.0
5
2
50 Pony 12 11 1 8.3
8 40 Otherst 94 94 0 0.0

PAL(-)-horses with lameness grade 0; PAL(+)-horses with

20
lameness grades 1 to 5.
Included any nonracing horse of mixed breeding, but which the
owner claimed to be of Thoroughbred extraction.
5 t Included breeds such as Hanovarian, Trakhener, Dutch Warm
Blood, etc.
$ Included breeds such as Appaloosa, American Saddlebred, Mor-
1 gan, draft, and grade.

1 I I I I 1 1 Utes or 50 for I 5 minutes. There was no significant asso-

10 20 30
ciation of post-anesthetic lameness with hypoxemia,
hypercarbia. or acidemia.
Hypotension Index (HI)

Fig. 2. This probit plot of the percentage of lame horses in column
(E), Table 3, depicts the effect of hypotension and its duration (hypo-
tension index or HI) on the development of post-anesthetic lameness
(PAL). From this graph (analogous to an LDSodetermination), the PAL
as influenced by the hypotension index (PAL/HI) 50 would occur at an
HI value of 20.0. A more reasonably acceptable incidence of 2% PAL
(PAL/HI 2) would likewise occur at an HI value of 4.0.
statistical significance in the occurrence of post-anes-
thetic lameness (Tables 4, 5). No statistical significance
was found for season of the year, administration of pre-
anesthetic or intraoperative drugs, techniques for induc-
tion or maintenance of anesthesia (Table 6), rate of fluid
administration, the procedure performed, or the recum-
bent position (Table 7).
Anesthetic duration was found to have a significant
association with post-anesthetic lameness (p < .OO 1 ) (Ta-
ble 7). The expected percentage of lameness after 2 hours
of anesthesia was 4.5% (Fig. 1) in this group of horses.
The PAL/AD 2 (2% incidence oflameness, as influenced
by anesthetic duration) was determined to be 1.6 hours.
The Significance of physiologic parameters is summa-
rized (Table 8). Hypotension was significant in the devel-
opment of post-anesthetic lameness ( p < .02). The hypo-
tension index that resulted in a post-anesthetic lameness
incidence of 2% (PAL/HI 2) was 4.0. Other similar data
can also be determined (Fig. 2). In horses with an H I
value of 5.0, the post-anesthetic lameness incidence
would be expected to be 2.570 (Fig. 2). This relatively
small HI value corresponds to an MAP of 60 for 30 min-
Discussion
The direct cause of post-anesthetic lameness appears
to be a decrease in perfusion to the muscles with resultant
local hypoxia, energy starvation, and other local meta-
bolic alteration^.^.^^'^^'^."^'^ Cardiovascular depression
and resultant systemic hypotension during maintenance
of general anesthesia also significantly affect the inci-
dence of myopathy.2'.' The influence of hypotension on
post-anesthetic lameness has been studied extensively,
with most findings supporting a relationship between
them.6.7.Y.10.1 ?.I3.I5.?2-?5 Hypotension and cardiovascular
depression during anesthetic maintenance are known to
reduce blood flow and muscle perfusion, which results in
myopathy in the form of post-anesthetic lameness. I"."
Mean arterial pressures below 55-65 mm Hg for more
than 30 minutes significantly increase the incidence of
TABLE 5. Contribution of lntrinsic factors to the Developmentof
Post-Anesthetic Lameness
Intrinsic Factor p Value
Breed 0.54 (ns)*
Weight 0 95 (ns)
Age 0 42 (ns)
Sex 0 97 (ns)
0 30 (ns)
Degree of fitness
History of exercise induced myopathy 0 42 (ns)
(ns)-no significant correlation with post-anesthetic lameness
396 EQUINE POST-ANESTHETIC LAMENESS

TABLE 6. Anesthetic lnduction and Maintenance Techniques Used TABLE 8. lnfluence of Physiologic Factors on the
Developmentof Post-AnestheticLameness
Induction
Thiamylal Physiologic Factor D Value
Guaifenesin and Thiamylal
Ketamine Hypotension (MAP < 70 mm Hg) 0.02
Guaifenesin and Ketamine Hypoxemia (PaO, < 100 mm Hg) 0.87 (ns)*
Inhalant Hypercarbia (PaCO, > 60 mm Hg) 0.66 (ns)
Maintenance Acidemia (pH, < 7.35) 0.63 (ns)
Halothane
lsoflurane (ns)-no significant correlation with post-anesthetic lameness.
lnjectables only

lameness in the post-anesthetic p e r i ~ d . ~ . ~ ’In

. ’ ~this
study, normotensive horses had a significantly lower in-
cidence of post-anesthetic lameness than hypotensive
horses (p < .02).
The hypotension index, which considers the degree
and the duration of hypotension, can be calculated and
plotted (Fig. 2). This plot can be used to predict the per-
centage of horses that will develop post-anesthetic lame-
ness at any given HI value. Hypotensive horses with
MAP of 60 mm Hg for 1 hour have HI values of 10.
Therefore, 10%of these horses would develop post-anes-
thetic lameness. However, only 3% of horses with MAP
of 60 mm Hg for 30 minutes should develop post-anes-
thetic lameness. Since the slope of this line is fairly steep
(48”), both the magnitude and the duration of hypoten-
sion are important determinants of the development of
post-anesthetic lameness.
By using the PAL/AD data (Fig. I). an estimate of the
percentage of horses that would develop post-anesthetic
lameness for a given anesthetic duration can be obtained.
From these data, an anesthetic duration of 2 hours would
result in a predicted post-anesthetic lameness incidence
of 4.5%. This prediction compares well with the pre-
viously reported post-anesthetic lameness incidence of
3.4%after 2 hours of anesthesia.’ In our population with
anesthetic durations of 0.13 to 7.00 hours, the incidence
of post-anesthetic lameness (6.4%) was slightly greater
TABLE 7. Contribution of Extrinsic Factors to the
Development of Post-AnestheticLameness
than the predicted incidence (4.5%)at 2 hours. This dis-
crepancy, which may not be significant, is in part due to
additional contributing factors (e.g., hypotension).
The length of time a horse is recumbent has been
shown to play an important role in the development of
post-anesthetic 2.14,’6.2y The findings of the
present study correlate well with those of other investiga-
tors who found that the duration of anesthesia contrib-
uted significantly to post-anesthetic lameness.’
To reduce the incidence of post-anesthetic lameness,
both variables (durations of anesthesia and hypotension)
must be considered. Anesthetic duration is relatively
fixed, but the surgeon can control length of anesthesia to
some degree by avoiding delays in the surgical prepara-
tion or the procedure. However, in unavoidably long
cases such as difficult fracture repairs, the duration of an-
esthesia will greatly increase the risk of post-anesthetic
lameness.
The second variable, hypotension, can be controlled
more readily by prompt and aggressive treatment
through the use of intravenous fluids, decreasing concen-
trations of inhalant anesthetics, and administration of
vasopressors or cardiotonics. Even at an MAP of 60 mm
Hg, the risk of post-anesthetic lameness increases with
the length of time this MAP is maintained. In a poten-
tially lengthy anesthetic, therefore, this relatively minor
degree of hypotension will serve to increase the risk of
post-anesthetic lameness greatly.
Despite clinical and anecdotal information in the liter-
ature that implicates many other factors, this study does
not suppofi such c ~ a i m s . ~ . ~ , ~ - i ~ . i ’ . i 4 - i 7 , i 9 . 2 ~ ~ ~Ith . ~had
9

Extrinsic Factor p Value been a clinical impression that choice of induction tech-
nique, degree of fitness, body size and type, and proce-
Season of the year 0.60 (ns)* dure influenced the risk of post-anesthetic lameness de-
Pre-anesthestic drugs 0.76 (ns)
Intraoperative drugs 0.19 (ns)
velopment. However, none of these factors was sup-
Induction technique 0.27 (ns) ported by our data. Although hypoxemia, hypercarbia,
Anesthetic maintenance technique 0.86 (ns) or acidemia did not contribute to the development of
Rate of IV fluid administration 0.75 (ns) post-anesthetic lameness, the relatively small number of
Duration of anesthesia 0.001 horses in the present study with post-anesthetic lameness
Procedure performed 0.12 (ns)
Recumbent position 0.79 (ns)
did not permit statistical analysis of the interaction of
these factors with hypotension, HI, or anesthetic dura-
* (ns)-no significant correlation with post-anesthetic lameness tion.
 RICHEY, HOLLAND, McGRATH, DODMAN, MARSHALL, COURT, NORMAN, AND SEELER
In conclusion, of the 19 factors studied, only the dura-
tion of anesthesia and hypotension contributed signifi-
cantly to post-anesthetic lameness. The best prevention,
therefore. is to maintain the MAP at 70 or more, treat
hypotension promptly, and most importantly, restrict
anesthetic time to the minimum needed to perform the
desired procedure.
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