342 EQUINE VETERINARY JOURNAL

Equine vet. J. (2005) 37 (4) 342-346

Summary
Reasons for performing study: The most common cause of death
as a direct result of colic is acute circulatory failure secondary
to intestinal ischaemia. Early and accurate recognition of
ischaemic bowel is essential to decrease complications and
increase survival. Blood to peritoneal lactate values have been
evaluated as a prognostic indicator, but lactate values
characterised by type of lesion have not been reported.
Hypothesis: Plasma and peritoneal lactate values are higher in
horses with intestinal ischaemia secondary to a strangulating
obstruction (ISSO).
Methods: Venous blood and peritoneal fluid were collected
sequentially from 20 clinically healthy horses and 189 horses
admitted for colic during a one-year period. Blood gas, pH,
electrolyte (K
+
, Na
+
, Ca
++
, Cl
-
), glucose and lactate values
were determined for blood and peritoneal fluid samples;
other values recorded for peritoneal fluid included gross
appearance, total protein and nucleated cell count.
Information regarding diagnosis, treatment and outcome
was retrieved from the medical records.
Results: Peritoneal and plasma levels of lactate were lower in
control compared to clinical cases. Horses with ISSO had a
higher peritoneal lactate value (8.45 mmol/l) than those with
nonstrangulating obstruction (2.09 mmol/l). Factors with the
strongest correlations with the presence of ISSO were
changes in the gross appearance of the peritoneal fluid and
values of peritoneal fluid chloride, pH and log
10
lactate.
Conclusions: Analysis of peritoneal fluid gross appearance, pH,
lactate and chloride can be used for diagnosis of ISSO.
Potential relevance: Peritoneal fluid lactate is a better
predictor of ISSO than blood lactate and may aid in early
detection of catastrophic peritoneal lesions such as intestinal
strangulation and rupture.
Introduction
Colic is an important cause of morbidity and mortality in horses
(Tinker et al. 1997), commonly requiring surgical intervention for
resolution of the primary problem. Approximately 50% of horses
referred to a major referral institution for colic required
emergency abdominal surgery (Hardy 2004). The most common
cause of death as a direct result of colic is due to acute circulatory
failure secondary to intestinal ischaemia or infarction (Parry
1986). Early and accurate recognition of an ischaemic segment of
bowel is essential to decrease complications and increase patient
survival (Arden and Stick 1988).
Lactate is the end product of glycolysis and is most commonly
elevated due to poor tissue perfusion and anaerobic glycolysis
associated with circulatory shock (De Backer 2003). Intestinal
ischaemia has a negative effect on cell membrane permeability,
with intracellular by-products such as lactate being released into
the systemic circulation and peritoneal cavity (Liao et al. 1995).
Detection of these biochemical markers in blood or peritoneal
fluid may assist in the early detection of ischaemic bowel injury in
clinical cases. Previous studies have evaluated peripheral blood
lactate as a preoperative prognostic and diagnostic tool in both
equine (Donawick et al. 1975; Moore et al. 1976; Parry et al.
1983a; Furr et al. 1995; Thoefner et al. 2000) and human
(DeLaurier et al. 1994) patients. Blood to peritoneal fluid lactate
ratios have also been evaluated as a prognostic indicator in equine
acute abdomen patients (Parry et al. 1983b,c). However,
peritoneal fluid lactate values have not, to our knowledge, been
characterised by location or type of intestinal lesion.
The purposes of our study were to determine whether blood
lactate values and peritoneal fluid lactate, electrolyte, bicarbonate
and glucose values are sensitive indicators of intestinal ischaemia
secondary to a strangulating obstruction (ISSO) in the equine acute
abdomen and to develop an equation by using logistic regression to
predict the probability of a horse with colic having ISSO.
Materials and methods
The study was performed on 20 clinically healthy (control) horses
and 189 horses admitted to the Veterinary Medical Teaching Hospital
at the University of California, Davis, for colic of intestinal origin
during a period of one year. The Animal Care Committee of the
University of California approved the protocol for this study. All
clinical cases had an initial physical examination that included
abdominal auscultation and percussion, per rectum examination,
nasogastric intubation, abdominal radiographs and abdominal
ultrasound. Venous blood was collected aseptically and submitted for
haematology and serum biochemistry. Peritoneal fluid was obtained
aseptically in the standing horse by using a stainless steel teat
cannula inserted through a small stab incision on or immediately to
the right of the linea alba. Venous blood and peritoneal fluid were
Evaluation of peritoneal fluid lactate as a marker of intestinal
ischaemia in equine colic
K. M. LATSON, J. E. NIETO*, P. M. BELDOMENICO

and J. R. SNYDER
Veterinary Medical Teaching Hospital and Department of Surgical and Radiological Sciences, School of Veterinary Medicine, University of
California, Davis, California, USA.
Keywords: horse; colic; equine; intestinal ischaemia; abdominocentesis; lactate
*Author to whom correspondence should be addressed.

Present address: Leahurst Veterinary Field Station, University of Liverpool, UK.

[Paper received for publication 24.01.05; Accepted 19.05.05]
K. M. Latson et al. 343
collected sequentially in glass tubes containing lithium heparin
(Vacutainer)
1
; blood was obtained anaerobically and peritoneal fluid
by gravity flow from the teat cannula. Blood-gases, pH, electrolytes
(K
+
, Na
+
, Ca
++
, Cl
-
), glucose and total lactate values were
determined for all blood and peritoneal fluid samples within 10 mins
of harvesting. All samples were determined by using automatic
multiprofile system equipment (ABL 700 Series)
2
. Other values
recorded for peritoneal fluid included gross appearance (clear, turbid
or serosanguinous), total protein and nucleated cell count. Individual
patient data collected from the medical record included age, sex,
breed, heart and respiratory rates, peripheral packed cell volume
(PCV), total protein, total nucleated cell count and capillary refill
time at admission to the clinic, duration of colic signs before
presentation, location and length of intestinal lesion, specific
diagnosis, presence of a strangulating obstruction at either surgery or
necropsy, necessity of surgical intervention for resolution of the
problem, treatment provided (medical vs. surgical) and outcome.
Horses that responded to medical treatment and had normal gross
appearance and total protein of the peritoneal fluid were considered
not to have ISSO. Horses with any 2 of the following 3 conditions
on presentation were excluded from the study: marked leucopenia
(WBC<2500 cells/l), diarrhoea (2 episodes of faeces too liquid to
be scooped with a shovel) or fever (rectal temperature >39.2C).
Horses determined to have concomitant primary kidney or liver
disease were excluded from the study.
Statistical analysis
According to skewness and kurtosis statistics, the distribution of
peritoneal and plasma values of lactate depart from normality, for
which logarithmic (log
10
) transformation was required. To measure
the strength of the association between peritoneal and plasma
lactate values, the Pearson correlation coefficient was performed
for horses with colic and controls. Every studied variable was
compared between horses with colic and controls by either
2
or
t test, with the exception of total number of nucleated cells and
Ca
++
, which required nonparametric analysis (Mann-Whitney test).
For horses with colic, the association between peritoneal and
plasma values of lactate and the independent variables was
determined by using the appropriate statistical test (t test, Kruskal-
Wallis test, one-way ANOVA followed by Tukeys post hoc test,
Mann-Whitney tests or Spearman rank correlation coefficient). A
logistic regression model was developed to predict the probability
of a horse with colic having ISSO by creating an initial maximum
model from the variables most closely associated with ISSO in
clinical colic cases. As peritoneal HCO
3
-
and pH were highly
correlated, the most strongly associated variable (pH) was chosen
to avoid collinearity problems. The continuous explanatory
variables were evaluated graphically for nonlinearity of the logit. If
a nonlinear relationship was detected, it was corrected by adding
the appropriate polynomial term. Subsequently, the model was
subjected to reduction by the likelihood ratio test, and therefore
only those significantly important for the goodness of fit were left
in the model. All 2-way interactions were added to the remaining
main effects, and then excluded if nonsignificant (P>0.05) by
likelihood ratio test. Goodness of fit of the resulting final model
was assessed by Hosmer-Lemeshows test (Hosmer and Lemeshow
2000) and by Nagelkerke R
2
(Nagelkerke 1991). The first was used
to determine whether predicted values and deciles of risk differed
significantly and the second to assess what percentage of the
response was explained by the variables in the equation.
Results
Dependent variables
Peritoneal fluid lactate values were determined for control (n = 20)
and clinical colic cases (n = 189). Plasma lactate values were not
recorded in the medical record for 20 horses with colic and
therefore could not be used in the analysis. One control horse had
an unrepeatable high initial plasma lactate and was not included in
the calculations. Peritoneal fluid and plasma values for lactate were
significantly lower in control horses (P<0.001) than in clinical
cases. Mean s.d. lactate (mmol/l) concentrations for control
horses were 0.60 0.19 and 0.90 0.53 for peritoneal fluid and
plasma, respectively; and for clinical cases were 4.00 4.63 and
3.00 3.62 for peritoneal fluid and plasma, respectively. A highly
positive correlation was observed between plasma and peritoneal
lactate values in controls (R
2
= 0.9) and clinical cases (R
2
= 0.7).
Independent variables
Categorical variables: Of the 189 clinical colic cases, 82 were
female and 117 male (11 intact and 96 geldings). Breed distribution
was Quarter Horse or Appaloosa (n = 69; 37%), Thoroughbreds
(n = 51; 27%), Arabians (n = 24; 13%), ponies or miniature horses
(n = 11; 6%), Warmbloods (n = 10; 5%) and other breeds (n = 24;
13%). The period for which horses had clinical signs of colic before
presentation was mean s.d. 22 29 h. Abdominal surgery was
necessary for resolution of the primary problem in
92/189 (48.7%) of horses with colic. Peritoneal fluid was clear in all
controls and in 82/189 (43.4%) clinical cases, and turbid or
serosanguinous in the other 107 (56.6%) horses. Horses admitted for
colic were 25 times more likely to have grossly abnormal peritoneal
fluid (turbid or serosanguinous) than control horses. Of the clinical
cases, 127/189 (67.2%) were discharged from the clinic and
62/189 (32.8%) were subjected to euthanasia. Of these 62 horses,
5 (8%) suffered severe post operative complications, 17 (27%) were
subjected to euthanasia while in surgery and 40 (65%) on
presentation or after a short course of intensive medical treatment
due to poor prognosis or cost associated with continued treatment.
The location and type of primary problem were reported in
126 cases; the rest were individuals with colic that responded to
medical treatment. The primary problem was located in the small
intestine (n = 43; 34%), ascending colon (n = 68; 54%) or in the
small colon (n = 15; 12%). Of the horses that did not respond to
medical treatment, ISSO was diagnosed in 27/43 (63%) with a lesion
in the small intestine, 8/68 (11%) with a lesion in the ascending colon
and 4/15 (27%) with a lesion in the small colon. Horses with a lesion
in the small intestine were more likely to have ISSO than horses with
a lesion on the large or small colon (P<0.001).
Continuous variables: Haemodynamic status of cases was
assessed on admission using vital signs, PCV, total protein value
and total nucleated cell count (values summarised in Table 1).
Values for other continuous variables are shown in Table 2.
Plasma and peritoneal fluid lactate values, peritoneal fluid total
protein and peritoneal fluid glucose content were increased
significantly in horses with colic. Peritoneal fluid chloride,
sodium, bicarbonate and pH values were significantly decreased
in horses with colic. No significant difference was found between
controls and clinical cases for peritoneal fluid nucleated cell
count, potassium and calcium.
344 Evaluation of peritoneal fluid lactate
Association between lactate and independent variables: Peritoneal
fluid and plasma lactate values were independent of the
individuals age and sex. Peritoneal fluid lactate was significantly
lower (P = 0.016) in Warmbloods compared with all other breeds,
but no significant difference was found in plasma lactate values
between breeds. There was no significant correlation between
duration of clinical colic signs or length of affected intestine and
peritoneal or plasma lactate values. Peritoneal and plasma lactate
values were significantly higher in colic cases with ISSO vs.
nonstrangulating obstruction for all intestinal sections except
small colon. Peritoneal fluid and plasma lactate values for each
lesion type and location are summarised in Table 3. Horses that
required surgery and those that needed an intestinal resection and
anastomosis had higher values of plasma and peritoneal lactate.
Horses that were discharged from the hospital had lower plasma
and peritoneal lactate values than those subjected to euthanasia on
presentation or during surgery.
Plasma lactate levels exceeded peritoneal fluid lactate (i.e.
peritoneal:plasma lactate ratio <1.0) less frequently as peritoneal
fluid lactate values increased. In horses with colic, 54/169 (32%) had
a peritoneal:plasma lactate ratio <1.0. The majority, 52/54 (96%),
had simple obstructions and 2 had an ischaemic lesion (large colon
torsion and small colon strangulating lipoma); 16/54 (30%) needed
surgery for correction of the primary problem. Three of the 16 horses
that required surgery were subjected to euthanasia without treatment
due to financial constraints (small colon strangulating lipoma,
enterolith and 180 large colon volvulus) and surgery was performed
on 13 horses. Two surgically treated horses with peritoneal:plasma
ratios <1.0 had large colon torsions and were subjected to euthanasia;
one intraoperatively due to guarded prognosis and one post
operatively due to development of colitis. Also treated surgically and
discharged from the hospital were 6 horses with enteroliths,
2 with small colon impactions and 3 with large colon displacements.
Of the remaining 38 horses, 36 were treated medically and
discharged from the hospital and 2 were subjected to euthanasia due
to cost of treatment. In total, 47/54 (87%) horses with lactate ratios
<1.0 were treated successfully and discharged from the clinic.
When peritoneal fluid was serosanguinous or turbid, values of
peritoneal and plasma lactate were significantly higher compared
to those in horses that had clear fluid. Values of lactate in
peritoneal fluid were 2.03 and 5.51 mmol/l for horses with clear
and cloudy or serosanguinous peritoneal fluid, respectively.
Plasma lactate values were 1.91 and 3.91 mmol/l for horses with
grossly normal and abnormal peritoneal fluid, respectively.
When the association between plasma and peritoneal fluid lactate
and the independent continuous variables in the peritoneal fluid were
evaluated, a positive correlation was observed for total protein, total
nucleated cells and sodium, a negative correlation for chloride,
bicarbonate and pH and no association for calcium, potassium and
glucose. However, when the type of lesion was included, a positive
significant correlation between peritoneal and plasma lactate and
glucose was observed only in horses with a nonischaemic lesion.
Best model to predict the presence of ISSO: Variables that were
originally included in the logistic regression model were: log
10
peritoneal lactate, total protein, Cl
-
, Na
+
, K
+
, HCO
3
-
and pH, horses
age, sex, type of colic and gross aspect of the peritoneal fluid. Only
4 variables remained in the final model: log
10
peritoneal lactate;
peritoneal fluid Cl
-
and pH; and aspect of peritoneal fluid (normal
TABLE 1: Comparison of selected case and plasma parameters with
lesion type on clinical admission for colic
ISSO NSO Rupture Other
Heart rate 64 18
a
52 15
b
72 19
a
50 14
b
(beats/min) (n = 36) (n = 85) (n = 9) (n = 50)
RR (breaths/min) 27 14
a
21 12
a
35 20
a
25 14
a
(n = 30) (n = 83) (n = 8) (n = 47)
CRT (secs) 2.6 0.81
a
2.1 0.58
b
3.2 0.70
a
2.2 0.51
b
(n = 27) (n = 74) (n = 7) (n = 45)
Packed cell volume 44 11.2
a
36 6.4
b
44 7.7
ac
37 8.1
bc
(%) (n = 34) (n = 81) (n = 8) (n = 47)
Total protein (g/l) 70.0 8.9
a
68.0 8.6
a
67.0 6.1
a
67.0 8.2
a
(n = 34) (n = 81) (n = 8) (n = 47)
Nucleated cell count 9.9 4.6
a
8.1 3.32
a
3.5 2.17
b
8.9 3.18
a
(10
3
cells/ul) (n = 30) (n = 72) (n = 7) (n = 42)
RR = respiratory rate, CRT = capillary refill time; n = no. horses; ISSO = intestinal
ischaemia secondary to strangulating obstruction; NSO = nonstrangulating
obstruction. Values (mean s.d.) were compared between groups and a
P value <0.05 was considered to be significant. Values with different
superscripts indicate statistical significance.
TABLE 2: Comparison of variables for peritoneal fluid from clinical colic
cases and control horses
Clinical cases Controls
Lactate (mmol/l) 4.0 4.63* 0.6 0.19
(n = 189) (n = 20)
Total protein (g/l) 25.0 14.4* 16.0 4.6
(n = 189) (n = 20)
Nucleated cell count (x 10
3
cells/l) 11.0 44.2 2.3 3.0
(n = 189) (n = 20)
Glucose (mmol/l) 6.77 2.55* 5.82 0.28
(n = 185) (n = 20)
Chloride (mmol/l) 102.5 4.35* 104.9 2.40
(n = 185) (n = 20)
Potassium (mmol/l) 3.6 .88 3.6 0.26
(n = 186) (n = 20)
Sodium (mmol/l) 132.3 3.24* 134.2 2.14
(n = 186) (n = 20)
Calcium (mmol/l) 1.23 0.20 1.30 0.12
(n = 186) (n = 20)
Bicarbonate (mmol/l) 31.6 7.33* 39.8 10.13
(n = 183) (n = 20)
pH 7.51 0.21* 7.65 0.17
(n = 185) (n = 20)
Values are reported as mean s.d. for the continuous variables in control
horses and clinical colic cases. *Significant difference (P<0.05) between
control and clinical cases.
TABLE 3: Peritoneal and plasma lactate values (mean s.d.) in terms of
lesion type and location
Peritoneal fluid lactate (mmol/l) Plasma lactate (mmol/l)
ISSO NSO ISSO NSO
All cases 8.45 5.52* 2.09 2.09 5.48 4.75* 2.03 2.04
(n = 39) (n = 87) (n = 32) (n = 85)
Small intestine 9.21 5.74* 2.31 1.13 6.04 5.31* 2.08 1.42
(n = 27) (n = 16) (n = 20) (n = 15)
Large intestine 8.09 5.20* 2.07 2.37 5.75 3.95* 2.02 2.28
(n = 8) (n = 60) (n = 8) (n = 59)
Small colon 4.08 2.43 1.93 1.54 2.18 1.13 1.92 1.41
(n = 4) (n = 11) (n = 4) (n = 11)
Ruptured viscus 8.02 6.10 2.95 2.12
(n = 9) (n = 7)
n = No. horses. Ruptured viscus was not found in association with
strangulating lesions in this study. ISSO = intestinal ischaemia secondary to
strangulating obstruction; NSO = nonstrangulating obstruction. *Significant
difference (P<0.05) between ISSO and NSO.
K. M. Latson et al. 345
vs. abnormal). Using the model, an equation was developed to
estimate the probability of a horse with colic having ISSO:
P = 1/1 + e
[(-146.84[log
10
AbLact] + 0.2874AbCl - 2.06AbpH - 1.823AbGross
+ 19.118[log
10
AbLact] * AbpH) - 9.85]
where P = probability of finding ISSO; log
10
AbLact = log
10
peritoneal fluid lactate; AbCl = peritoneal fluid Cl
-
(mmol/l);
AbpH = peritoneal fluid pH; AbGross = presence of clear
peritoneal fluid (0) or presence of cloudy or serosanguinous
peritoneal fluid (1); and AbLact = value of peritoneal lactate
(mmol/l). The final model showed a Nagelkerke R
2
(Nagelkerke
1991) of 0.756 and a Hosmer-Lemeshow goodness of fit (Hosmer
and Lemeshow 2000) of 0.947 (the maximum possible being 1).
Discussion
Basal plasma lactate values are <2 mmol/l in horses (Lumsden et
al. 1980; Moore et al. 1980; Flisinska-Bojanowska et al. 1991)
and peritoneal fluid lactate concentrations of 0.7 0.2 and
0.66 0.43 mmol/l have been reported (Moore et al. 1977; Parry
and Crisman 1991). Plasma lactate is always higher in normal,
resting horses than peritoneal fluid lactate (Moore et al. 1977).
Plasma and peritoneal fluid lactate values in our control horses
were similar to previously reported values.
Biochemical markers such as creatine kinase (primarily a
seromuscular enzyme) and lactate (formed in cells of all intestinal
wall layers) released after experimentally induced bowel
ischaemia of rabbits become elevated in peritoneal fluid sooner
and to a greater extent than in blood (Liao et al. 1995). A similar
progressive relationship between blood and peritoneal fluid lactate
concentrations has been postulated for clinical cases of equine
colic (Parry 1987). Peritoneal lactate remains lower than plasma
lactate throughout the initial stages of mild ischaemia, after which
peritoneal lactate becomes higher. As ischaemia progresses,
peritoneal fluid lactate levels rise more quickly than blood lactate
in the haemodynamically stable patient, resulting in progressive
disparity between values; this is thought to be due to the peritoneal
membranes large surface area, which filters small molecules
(such as lactate) into the peritoneal cavity but has low
permeability to larger proteins (Liao et al. 1995). With onset of
concurrent systemic shock, blood lactate values rise steeply to
approach peritoneal fluid lactate levels.
In the study reported here, and as previously reported by Parry
et al. (1983c), a high positive correlation between plasma and
peritoneal lactate was observed in horses with colic. The
difference between peritoneal and plasma lactate values offers a
sensitive and specific means for detecting ruptured viscus and
necrotic intestine in man (DeLaurier et al. 1994) and for
differentiating between septic and nonseptic peritonitis in dogs
(Bonczynski et al. 2003; Levin et al. 2004).
Similar peritoneal:plasma lactate ratios have been evaluated for
prognostic purposes in horses with colic. The results of these studies
showed that all horses having lactate values higher in plasma than
in peritoneal fluid survived (Moore et al. 1977; Parry et al. 1983c).
However, the number of horses in the previously mentioned studies
were limited to <7. Thoefner et al. (2000) showed a decreased need
for surgical treatment of horses with peritoneal:plasma lactate ratios
<1.0. Peritoneal:plasma lactate ratio <1.0 in this study did not offer
a sensitive means for determining a horses need for surgery, but
was most often found in horses with simple obstructive intestinal
lesions. Compared to horses with ISSO in this study, the less severe
haemodynamic alterations and lack of compromised intestine found
with simple obstructive lesions explain this finding.
Characterisation of peritoneal fluid lactate concentrations
based on the presence of ISSO has not, to our knowledge, been
reported. The presence of a strangulating obstruction and grossly
affected intestine observed at surgery or necropsy was
considered to be consistent with ISSO in our study. Severity of
tissue deterioration due to ischaemia was not evaluated
histologically as a primary cause of elevated lactate levels.
However, one study showed that changes in plasma and
peritoneal fluid correlated well with histological scores of bowel
injury in rabbits (Liao et al. 1995). The evaluation of similar
histological analysis may have accounted for higher lactate
concentrations in short bowel segments and vice versa. In
strangulating small intestinal lesions, progressive distension
proximal to the primary lesion obstructs venous outflow,
eventually compromising arteriolar and mesenteric blood flow
(Dabareiner et al. 2001), and may have contributed to elevated
lactate values. A similar low-flow state may be present during
the early phases of large colon strangulation/volvulus (Snyder et
al. 1990) and secondary luminal distension (Ruf et al. 1980),
with blood being shunted away from the colonic mucosa and
increasing ischaemic injury to the tissues.
Although intestinal mucosa produces some lactate from
glycolysis under aerobic conditions, ischaemic intestine is
probably the most important source of lactate in horses with colic
(Ruggles et al. 1993). Hepatic clearance of lactate accounts for
approximately 50% of lactate metabolism (Vail et al. 1990). Other
sites of clearance include the renal cortex (30%) and hepatic, brain
and myocardial cells, which anaerobically metabolise lactate (De
Backer 2003). Horses determined to have primary renal or hepatic
disease were excluded from this study. Several horses included in
this study had mild prerenal azotaemia on presentation that
resolved in all cases with i.v. crystalloid fluid administration;
therefore, increased lactate concentration as a primary failure of
metabolism or clearance was unlikely.
Decreased sodium, chloride and bicarbonate concentrations in
the peritoneal fluid of horses with colic vs. controls may be, in
part, due to equilibration with the increased volume of peritoneal
fluid in clinical colic cases (Swanwick and Wilkinson 1976).
Experimentally, peritoneal fluid production rate increased 10-fold
within 30 h of colon infarction (Nelson et al. 1968). Decreased
chloride and bicarbonate concentrations were inversely correlated
with lactate values in peritoneal fluid and slightly less with
elevated plasma lactate values. These electrolyte and bicarbonate
abnormalities function to offset increased lactate levels by
maintaining anion balance and, in large part, contribute to the
previously reported increases in anion gap and metabolic acidosis
that occur in colic cases (Parry 1987). Decreased peritoneal pH
values were, as a result, also highly associated with elevated
peritoneal and plasma lactate values.
Serum glucose elevations have been reported in horses after
excitement, transportation, stress, pain and acute, severe colic.
Endogenous corticosteroids and catecholamines are thought to
mediate systemic glucose elevations. Elevated serum glucose has
been described in the initial phases of endotoxaemia and glucose
values >13.9 mmol/l have been associated with poor prognosis in
equine colic. Significant elevations of peritoneal fluid glucose
concentrations in clinical colic cases compared with controls
could be a consequence of any of these factors.
346 Evaluation of peritoneal fluid lactate
Peritoneal fluid colour was the most important variable
associated with the need for surgical intervention (Matthews et al.
2002) and had a high positive predictive value for lesion type
(strangulating vs. nonstrangulating) (Freden et al. 1998). In our
study, peritoneal fluid was dichotomised by the technician
performing the measurements into clear vs. not clear (turbid,
serosanguinous, grossly feed-contaminated) by comparing the
clinical sample to that of a grossly and clinicopathologically normal
sample from a control horse. The mean peritoneal fluid lactate value
was significantly higher (5.51 mmol/l) when peritoneal fluid was
not clear than when it was (2.03 mmol/l). Plasma lactate was also
elevated, but not as significantly or by as great a magnitude.
Increased peritoneal and plasma lactate values have a direct,
predisposing association with the need for surgery in clinical colic
cases (Thoefner et al. 2000), but are not useful if isolated from
other correlating clinical and laboratory data. Multivariable models
have been developed to predict need for surgery, lesion site and
prognosis for horses with abdominal pain (Freden et al. 1998;
Orsini et al. 1988). Our study has shown that a logistic regression
model using peritoneal fluid lactate, chloride and pH values and
peritoneal fluid gross appearance can be used to calculate a
prognostic index for the presence of intestinal ischaemia secondary
to strangulating obstruction very accurately. Of 48 strangulating
intestinal lesions, 39 (81.25%) had a predictive value of >60%
using the model; by contrast, of 122 nonstrangulating lesions in
horses with abdominal pain, 104 (85%) had a predictive value of
<60%. Because peritoneal and plasma lactate values may be
elevated due to metabolic disturbances other than the acute
abdomen, this model should be validated on a large, second set of
data prior to application in general practice and should be used as
a correlate to clinical signs for each case. Additionally, large
variances in predictive value for strangulation can be obtained by
incorrect categorisation of peritoneal fluid as clear or not clear.
The results of this study suggest that ISSO can produce
significant elevations in peritoneal fluid lactate values, which closely
correlate with other physical and biochemical changes in peritoneal
fluid. Paired analysis of peritoneal and plasma lactate values may
offer more insight into cardiovascular and systemic function than
peritoneal fluid values alone. Use of the predictive model for presence
of intestinal necrosis as an adjunct to clinical case presentation may
provide earlier diagnosis, quicker definitive treatment and decreased
morbidity in cases of strangulating intestinal lesions.
Manufacturers addresses
1
Sherwood Medical, St. Louis, Missouri, USA.
2
Radiometer Copenhagen, Bronshoj, Denmark.
References
Arden, W.A. and Stick, J.A. (1988) Serum and peritoneal fluid phosphate
concentrations as predictors of major intestinal injury associated with equine
colic. J. Am. vet. med. Ass. 193, 927-931.
Bonczynski, J.J., Ludwig, L.L., Barton, L.J., Loar, A. and Peterson, M.E. (2003)
Comparison of peritoneal fluid and peripheral blood pH, bicarbonate, glucose,
and lactate concentration as a diagnostic tool for septic peritonitis in dogs and
cats. Vet. Surg. 32, 161-166.
Dabareiner, R.M., White, N.A. and Donaldson, L.L. (2001) Effects of intraluminal
distention and decompression on microvascular permeability and hemodynamics
of the equine jejunum. Am. J. vet. Res. 62, 225-236.
De Backer, D. (2003) Lactic acidosis. Intensive Care Med. 29, 699-702.
DeLaurier, G.A., Ivey, R.K. and Johnson, R.H. (1994) Peritoneal fluid lactic acid and
diagnostic dilemmas in acute abdominal disease. Am. J. Surg. 167, 302-305.
Donawick, W.J., Ramberg, C.F., Paul, S.R. and Hiza, M.A. (1975) The diagnostic and
prognostic value of lactate determinations in horses with acute abdominal crisis.
J. S. Afr. vet. Ass. 46, 127.
Flisinska-Bojanowska, A., Gill, J. and Komosa, M. (1991) Diurnal changes in lactic
and pyruvic acid levels and pH values in foals during the first 13 weeks of their
life and in their lactating mothers. Comp. Biochem. Physiol. A 99, 113-117.
Freden, G.O., Provost, P.J. and Rand, W.M. (1998) Reliability of using results of
abdominal fluid analysis to determine treatment and predict lesion type and outcome
for horses with colic: 218 cases (1991-1994). J. Am. vet. med. Ass. 213, 1012-1015.
Furr, M.O., Lessard, P. and White, N.A. (1995) Development of a colic severity score
for predicting the outcome of equine colic. Vet. Surg. 24, 97-101.
Hardy, J. (2004) Design and organization of an equine intensive care unit. Vet. Clin.
N. Am.: Equine Pract. 20, 1-10.
Hosmer, D.W. and Lemeshow, S. (2000) Applied Logistic Regression, 2nd edn.,
Wiley, New York.
Levin, G.M., Bonczynski, J.J., Ludwig, L.L., Barton, L.J. and Loar, A.S. (2004)
Lactate as a diagnostic test for septic peritoneal effusions in dogs and cats. J. Am.
anim. hosp. Ass. 40, 364-371.
Liao, X.P., She, Y.X., Shi, C.R. and Li, M. (1995) Changes in body fluid markers in
intestinal ischaemia. J. Pediatr. Surg. 30, 1412-1415.
Lumsden, J.H., Rowe, R. and Mullen, K. (1980) Hematology and biochemistry
reference values for the light horse. Can. J. Comp. Med. 44, 32-42.
Matthews, S., Dart, A.J., Reid, S.W., Dowling, B.A. and Hodgson, D.R. (2002)
Predictive values, sensitivity and specificity of abdominal fluid variables in
determining the need for surgery in horses with an acute abdominal crisis. Aust.
vet. J. 80, 132-136.
Moore, J.N., Owen, R.R. and Lumsden, J.H. (1976) Clinical evaluation of blood
lactate levels in equine colic. Equine vet. J. 8, 49-54.
Moore, J.N., Garner, H.E., Shapland, J.E. and Hatfield, D.G. (1980) Lactic acidosis
and arterial hypoxemia during sublethal endotoxemia in conscious ponies. Am. J.
vet. Res. 41, 1696-1698.
Moore, J.N., Traver, D.S., Turner, M.F., White, F.J., Huesgen, J.G. and Butera, T.S.
(1977) Lactic acid concentration in peritoneal fluid of normal and diseased
horses. Res. vet. Sci. 23, 117-118.
Nagelkerke, N.J.D. (1991) A note on the general definition of the coefficient of
determination. Biometrika 78, 691-692.
Nelson, A.W., Collier, J.R. and Griner, L.A. (1968) Acute surgical colonic infarction
in the horse. Am. J. vet. Res. 29, 315-327.
Orsini, J.A., Elser, A.H., Galligan, D.T., Donawick, W.J. and Kronfeld, D.S. (1988)
Prognostic index for acute abdominal crisis (colic) in horses. Am. J. vet. Res. 49,
1969-1971.
Parry, B.W. (1986) Prognostic evaluation of equine colic cases. Comp. cont. Educ.
pract. Vet. 8, S98-S104.
Parry, B.W. (1987) Use of clinical pathology in evaluation of horses with colic. Vet.
Clin. N. Am.: Equine Pract. 3, 529-542.
Parry, B.W. and Crisman, M.V. (1991) Serum and peritoneal fluid amylase and lipase
reference values in horses. Equine vet. J. 23, 390-391.
Parry, B.W., Anderson, G.A. and Gay, C.C. (1983a) Prognosis in equine colic: a
comparative study of variables used to assess individual cases. Equine vet. J. 15,
211-215.
Parry, B.W., Anderson, G.A. and Gay, C.C. (1983b) Prognosis in equine colic: a study
of individual variables used in case assessment. Equine vet. J. 15, 337-344.
Parry, B.W., Gay, C.C. and Anderson, G.A. (1983c) Assessment of the necessity for
surgical intervention in cases of equine colic: a retrospective study. Equine vet.
J. 15, 216-221.
Ruf, W., Suehiro, G.T., Suehiro, A., Pressler, V. and McNamara, J.J. (1980) Intestinal
blood flow at various intraluminal pressures in the piglet with closed abdomen.
Ann. Surg. 191, 157-163.
Ruggles, A.J., Freeman, D.E., Acland, H.M. and FitzSimmons, M. (1993) Changes in
fluid composition on the serosal surface of jejunum and small colon subjected to
venous strangulation obstruction in ponies. Am. J. vet. Res. 54, 333-340.
Snyder, J.R., Pascoe, J.R., Olander, H.J., Hinds, D.M., Young, R. and Tyler, W.S.
(1990) Vascular injury associated with naturally occurring strangulating
obstructions of the equine large colon. Vet. Surg. 19, 446-455.
Swanwick, R.A. and Wilkinson, J.S. (1976) A clinical evaluation of abdominal
paracentesis in the horse. Aust. vet. J. 52, 109-117.
Thoefner, M.B., Ersboll, A.K. and Hesselholt, M. (2000) Prognostic indicators in a
Danish hospital-based population of colic horses. Equine vet. J., Suppl. 32, 11-18.
Tinker, M.K., White, N.A., Lessard, P., Thatcher, C.D., Pelzer, K.D., Davis, B. and
Carmel, D.K. (1997) Prospective study of equine colic incidence and mortality.
Equine vet. J. 29, 448-453.
Vail, D.M., Ogilvie, G.K., Fettman, M.J. and Wheeler, S.L. (1990) Exacerbation of
hyperlactatemia by infusion of lactated Ringers solution in dogs with
lymphoma. J. vet. intern. Med. 4, 228-232.