Page 10 - Basic Monitoring in Canine and Feline Emergency Patients

Table 1.1. Normal reference range for blood glucose hyponatremia). Typically, glucosuria (and volume
during the resting state in dogs and cats. loss through the kidneys) starts to occur in dogs and
VetBooks.ir Species Normal reference range (mg/dL) cats when the serum glucose exceeds 180–200 mg/
dL and 260–310 mg/dL, respectively. Hyperglycemia
has also been linked to other deleterious conse-
Canine
80–140
Feline 80–120 quences such as immunosuppression, increased
inflammation, disruption of normal coagulation,
and alterations of the endothelium.
insulin opposed by the counter-regulatory hor-
mones glucagon, cortisol, epinephrine, and growth Ketone levels
hormone. These hormones can stimulate further glu-
cose release into the bloodstream to maintain or Ketones are produced as a consequence of fat store
increase BG levels. When glucose is not maintained metabolism. While ketosis can occur with other
under tight control, hypoglycemia or hyperglyce- disease states such as hepatic lipidosis, starvation,
mia can occur. Both conditions can be affiliated or errors of metabolism, the most common situa-
with morbidity and mortality. tion in veterinary patients in which measurement of
The brain is an obligate glucose user and has ketones is important is in patients suspected or
reduced or minimal capabilities to liberate its own known to have diabetes mellitus. Diabetic ketoaci-
glucose from glycogen stores or to use protein as an dosis (DKA) is a life-threatening complication of
energy source. Therefore, the brain relies on sys- diabetes mellitus marked by hyperglycemia with
temic delivery of glucose to maintain normal meta- excessive ketone production and subsequent acido-
bolic function. Thus, when hypoglycemia occurs, sis from the ketones. In DKA, a lack of insulin
not only are the majority of clinical signs associ- production and/or lack of insulin binding to its
ated with insufficient glucose delivery to the brain receptors on cells coupled with an increase in
(neuroglycopenia), but they also occur within a counter-regulatory hormones including glucagon,
relatively short period of time. If the hypoglycemia epinephrine, glucocorticoids, and growth hormone
is not corrected quickly or is allowed to persist for leads to an increase in glucose levels within the
an extended period of time, these neurologic- bloodstream. In addition, free fatty acid (FFA)
related clinical signs may persist beyond the time of breakdown increases in response to the counter-
correction and may progress to include cortical regulatory hormones in an attempt to create more
blindness and peripheral nerve demyelination. glucose and provide more energy to the cells. The
Hyperglycemia can be tolerated for longer peri- excessive amount of FFAs presented to the cells
ods of time with the more minor increases in BG overwhelm their ability to oxidize these FFAs to
(<200 mg/dL) typically not leading to clinical signs acetyl coenzyme A to enter the TCA cycle and
and hence able to be tolerated for longer periods of undergo aerobic metabolism to ATP. Instead, the
time. Severe hyperglycemia (>200 mg/dL) is associ- excess FFAs are oxidized to ketone bodies that are
ated with clinical signs and is not tolerated for long released into the circulation.
periods. The most common clinical signs in the There are three ketone bodies that are formed
case of hyperglycemia are associated with fluid during this process: acetoacetate, 3-betahydroxy-
losses. This is due to the fact that significant hyper- butyrate (3-HB), and acetone. Of these, acetoace-
glycemia causes fluid to shift into the vascular tate is produced first from the oxidation of FFAs; it
space from the cells. Large quantities of glucose is then reduced in the mitochondria to yield 3-HB.
molecules act as an effective osmole and draw Acetone is produced from the decarboxylation of
water from the cells into the vasculature. These acetoacetate. Acetone is produced in the smallest
fluid shifts lead to cellular dehydration. At the quantities and acetoacetate and 3-HB, the two
same time, the glucose molecule will similarly major ketone bodies in animals, are normally pre-
retain water with it in the renal tubules, leading to sent in equal proportions. However, in animals
polyuria. Significant polyuria can cause enough with DKA, 3-HB can be produced in amounts five
fluid and concurrent electrolyte loss via the urinary to ten times those of acetoacetate. Once insulin
system to lead to further cellular dehydration and therapy is initiated, the levels of 3-HB will decrease
electrolyte deficiencies (especially hypokalemia and more rapidly than acetoacetate concentrations.

2 P.A. Johnson