Page 402 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

392 FLUID THERAPY

individual patient may result in weight loss, and exces- indications of inadequate perfusion or tissue hypoxia
8
sive intravenous fluid administration may result in are present. Type A hyperlactatemia also includes relative
unnecessary weight gain. hypoxia, in which energy requirements exceed demand
such as may occur in strenuous exercise and in extreme
PERFUSION muscle activity (e.g., seizures, trembling, struggling). 35
This effect resolves rapidly after cessation of the activity.
LACTATE Acid-Base Status
The blood lactate concentration may be used as an indi- Many illnesses and trauma are associated with acid-base
cator of perfusion to monitor resuscitation and is disturbances, often, metabolic acidosis. Hypoperfusion
discussed further in Chapter 10. Strict adherence to and tissue hypoxia result in metabolic acidemia unless a
collection (i.e., blood should be collected in heparin) comorbid condition results in metabolic alkalosis,
and processing (i.e., immediate) of blood samples is generating a mixed disturbance in which blood pH may
required. Lactate measurements can be performed be within normal limits. In one study, 95% of animals
on arterial or venous samples. 34,43 Normal blood lactate referred to a tertiary referral center were diagnosed with
concentrations are less than 2.0 mmol/L in dogs, with 3 metabolic acidosis. 41 Knowing the metabolic status of a
to 5 mmol/L representing a mild increase, 5 to 8 mmol/ patient is an extremely important part of the overall
L a moderate increase, and more than 8 mmol/L a severe assessment of the animal and provides information about
increase. Normal blood lactate concentrations are less the potential origin of the abnormality and the appropri-
than 1.46 mmol/L in cats. When inadequate oxygen ate fluid to select. Eliminating the underlying problem
delivery to tissues occurs, cells revert to anaerobic metab- ultimately will correct the abnormal metabolic status,
olism, and lactate production increases. Obtaining an ini- but until it can be resolved, providing optimal therapy
tial lactate measurement in all severely ill patients can to improve outcome is essential. When blood gas analysis

serve as a useful method of evaluating severity of illness is not available, acidemic patients with HCO 3 loss usu-
or injury. This was illustrated in a recent study of blunt ally can be identified as having increased serum chloride
trauma in dogs. 74 Monitoring lactate concentrations as concentration, decreased total CO 2 , and normal anion
a method of measuring total body oxygen metabolism gap, information that can be obtained from a serum bio-
will provide information about the state of oxygen deliv- chemistry profile. If acidemia is caused by the addition of
ery and adequacy of resuscitation. With restoration of an unmeasured anion (e.g., lactate, glycolate), the serum
adequate perfusion and oxygen delivery, aerobic metabo- chloride concentration usually is normal, but the anion
lism is resumed with a reduction in lactate production. A gap is increased. Where inappropriate administration of
recent study in human septic patients demonstrated that 0.9% sodium chloride is administered, a hyperchloremic
lactate clearance derived from calculating the change in metabolic acidosis frequently occurs. Alkalemic patients,
lactate concentration from two blood samples drawn at however, often are hypochloremic. Monitoring acid-base
two time points (before and after treatment [e.g., fluid status provides additional information about improved
bolus]) was not inferior to ScvO 2 measurements as a perfusion and resolution of the illness, as well as the
marker of adequacy of oxygen delivery. A lactate clearance potential need for a change in fluid therapy as the disease
of more than 10% ([lactate initial—lactate resuscitation/ process changes. For example, a dog with vomiting
lactate initial]/100%) may be a useful monitoring tech- caused by pyloric obstruction commonly will exhibit a
nique in assessing improved perfusion status, especially hypochloremic metabolic alkalosis and hyponatremia;
in situations where appropriate equipment is not available 0.9% sodium chloride is the fluid of choice. Once the
to measure saturation of oxygen in central venous or jug- underlying problem is resolved and alkalosis has been
ular vein samples. 40 corrected, continuing with 0.9% sodium chloride may
The most common cause of hyperlactatemia is result in hyperchloremic acidosis; therefore a change to
hypoperfusion and tissue hypoxia (type A), but increased a balanced electrolyte solution typically is recommended.
lactate concentrations also may be caused by increased
production secondary to alkalosis, hypoglycemia, various HYDRATION
9
drugs, and systemic illness (type B). As an example, in Physical findings used to assess hydration are skin turgor,
those with acute liver failure and sepsis, hyperlactatemia position of the globes within the orbits, and moistness of
is not necessarily associated with hypoxia. In this situa- mucous membranes (see Table 16-1). 10 Assessment of
tion, the liver becomes a net producer of both lactate these findings should be noted on admission; however,
and pyruvate. 8 Similarly, in those with sepsis, there are confounding factors of the assessment which
hyperlactatemia is a consequence of enhanced glycolysis must be considered (see Table 16-2) when calculating
and increased release of lactate from the intestine and volume requirements to avoid overestimates and
the periphery. Therefore hypermetabolism must be con- underestimates. However, frequent monitoring of these
sidered as a cause for hyperlactatemia when no other findings is useful when monitoring response to therapy