GDV and Lactate
Stacy D. Meola, MS, DVM, DACVECC
In 1999 De Papp published a landmark paper in JAVMA
evaluating serum lactate levels in dogs with gastric dilation
and volvulus (GDV). The primary goal of the paper was to
establish a serum lactate level that would reliably predict
the presence of gastric necrosis as well as patient survival.
The results suggested that serum lactate >6.0 mmol/L predicted gastric necrosis with a moderately low sensitivity
(61%) and specificity (88%). They also showed that if the
lactate was <6 mmol/L, 99% of dogs survived. Until recently this paper has remained the standalone evaluation of lactate as a predictor of gastric necrosis and survival in dogs
with GDV.
In normal body conditions, with appropriate tissue perfusion and oxygenation, the default is aerobic metabolism. In
this normal situation glucose is converted during glycolysis
into pyruvate which then enters the Krebs cycle and through
oxidative phosphorylation creates ATP for energy. Oxygen
is an essential component for pyruvate to enter into the
Krebs cycle. In circumstances of circulatory compromise
there is resultant poor perfusion and inadequate oxygenation where the tissues instead default to anaerobic metabolism. In this environment, instead of ATP production, pyruvate is converted to two lactate molecules by the enzyme
lactate dehydrogenase. It is this lactate which we measure
as a reliable marker of anaerobic metabolism.
As the stomach dilates in dogs with GDV, it begins to lose
local perfusion and often undergoes necrosis. Concurrently
there is an increase of intra-abdominal pressure such that
perfusion is compromised to all abdominal organs. In severe
cases, venous return to the heart is reduced from caudal
vena cava compression by the stomach. Global perfusion is
further compromised from dehydration, vasodilation and
hypovolemic shock. The global hypoperfusion results in
cellular anaerobic metabolism and increased peripheral
lactate levels. If it were only the stomach that was poorly
oxygenated and compromised in a patient with GDV, then a
single pre-operative lactate level would be useful in predicting necrosis and survival. The flaw in De Papp’s paper is
that since metabolic changes in the stomach are only a
small component of the patients overall cellular hypoxia
and resultant lactate formation, it is wrong to assume it is a
specific reflection of changes in the stomach.
In 2010, Zacher evaluated the change in pre-operative lactate levels from the time of presentation to those following
gastric decompression and fluid resuscitation (JAVMA). The
results showed that if the patient’s perfusion and cellular
oxygenation could be improved through decompression of
the stomach and aggressive fluid administration there was a
decrease in serial lactate levels and increased survival.
There were three key findings in this study: 1. If the final
lactate was less than 6.4 mmol/L there was a 91% patient
survival rate. 2. If the lactate decreased by at least 4 mmol/L
there was an 86% patient survival rate. 3. If the percentage
change in serum lactate was greater than 42.5% there was
100% patient survival. These findings are likely to be very
helpful to the clinician as they represent whether or not the
patient is able to respond to treatment at the cellular level
and takes into account the patient’s global tissue oxygenation status. Unfortunately this publication was not helpful in
the prediction of gastric necrosis.
In a 2011 paper, Green used serial lactate changes in an
attempt to predict gastric necrosis as well as survival. One
of several limitations of this study was that the serial lactates
were not done pre-operatively. Instead they were evaluated
within the first 12 hours of ho spitalization. The established
cut off serum lactate value used as a predictor was unreliable. The results suggested that a serum lactate greater than
2.9 mmol/L (reference range (0.3-2.2 mmol/L) predicted gastric necrosis with a high sensitivity 93.8% but a very poor
specificity of 42.6%. The lactate cut off that was only 0.7
mmol/L higher than the reference range which is much too
close to normal to be useful. Furthermore, they claimed no
significant difference in survival patients that had a lactate
greater than 6 mmol/L. However, only 25% of dogs that had
a lactate greater than 6 mmol/L survived. One useful bit of
information in the study showed that a decrease in serial
serum lactate of greater than 50% from baseline resulted in
a 70% survival rate.
In the last 14 years we have gained some insight into the
usefulness of serum lactate analysis for prediction of overall
patient survival in dogs with GDV. It appears that aggressive
intervention which rapidly reestablishes adequate tissue
perfusion and oxygenation is the best method to improve
survival and can be tracked by monitoring serum lactate
levels. Unfortunately, lactate testing is still not able to reliably predict gastric necrosis. Abdominal exploratory surgery
remains the most useful modality for that determination.
The utility of serum lactate for evaluation of tissue perfusion
and gastric necrosis in GDV patients is still evolving and the
only thing that can accurately be stated is that there will be
more studies in the future.
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3 • WRVS’ Newsletter • March/April 2014