Page 139 - Clinical Small Animal Internal Medicine

13 Hypoglycemia in Patients without Diabetes Mellitus 107

thorough physical examination, thoracic and abdominal Critical Illness and Hypoglycemia: Renal
VetBooks.ir radiographs, abdominal ultrasonography, and histo­ Failure, Acquired Liver Disease, Sepsis,
and Virulent Babesiosis
pathologic examination of the tumor, which is often
located in the abdominal cavity.
Renal Failure
Renal failure is associated with hypoglycemia in critically
Treatment ill diabetic and nondiabetic human patients, but the
The long‐term therapeutic strategies in NICTH involve impact of renal failure on the blood glucose concentra­
complete removal of the tumor or reduction of the tion is unpredictable in dogs and cats. In most cases, the
tumor mass. In order to treat hypoglycemia, a short‐ blood glucose concentration is normal. However, hyper­
term beneficial effect is best achieved with (continu­ glycemia may develop as a result of uremic‐induced car­
ous) parenteral administration of glucose and dietary bohydrate intolerance and insulin resistance in a dog or
guidelines. Glucocorticoids, at least in humans, seem cat with impaired insulin secretion; this phenomenon
to be the most effective form of medical therapy in has been referred to as “pseudodiabetes.” Alternatively,
terms of long‐term relief from hypoglycemia by stimu­ renal failure may induce hypoglycemia.
lating glyconeogenesis and suppressing, although not Several mechanisms for the development of hypoglyce­
in all cases, the production of “big”‐IGF‐2. In addition, mia during renal insufficiency have been proposed. These
moderate to high doses of glucocorticoids may cause include reduced renal gluconeogenesis and decreased
shrinkage of the tumor. caloric intake related to inappetence. Normally, renal glu­
coneogenesis may supply as much as 45% of new glucose
during prolonged starvation. Additional defects in glu­
Hypoadrenocorticism cose homeostasis occur in renal insufficiency, including
Incidence an increased insulin half‐life related to decreased renal
Hypoadrenocorticism should always be on the rule‐out degradation or excretion of insulin, impaired hepatic gly­
list for hypoglycemia. Of 506 dogs diagnosed with cogenolysis and gluconeogenesis, inadequate glucose
hypoadrenocorticism at UC Davis Veterinary Medical counterregulatory responses, or a combination of these
Teaching Hospital, 116 (25%) were hypoglycemic at the factors. It should be emphasized that hypoglycemia is
time of diagnosis. Interestingly, however, clinical signs rarely the cause of death in the critically ill patient with
attributable to hypoglycemia appear to be uncommon. renal failure and is considered more a marker for multi­
In this cohort of cases, hypoglycemic seizures and other system failure than a cause of mortality.
clinical signs that may have been caused by hypoglyce­
mia, such as ataxia and disorientation, were observed in Acquired Hepatic Dysfunction
only 30 dogs (6%). Hypoglycemia has been associated with a wide spectrum
of liver diseases in people. These disorders include eve­
Pathophysiology and Treatment rything from type 1 glycogen storage disease, cirrhosis,
With glucocorticoid deficiency, glucose production by viral hepatitis, procainamide‐induced hepatitis, chole­
the liver (i.e., gluconeogenesis) is decreased and the sen­ cystitis, and metastatic infiltration to fulminant liver fail­
sitivity of insulin receptors in peripheral tissues is ure after cardiac arrest. In dogs and cats, hypoglycemia
increased. In tandem, these factors predispose the ani­ often results from severe destruction of the liver from
mal with adrenal insufficiency to hypoglycemia. That bacterial infection, hepatotoxins, neoplasia, and chronic
said, the blood glucose concentration should always be fibrosis/cirrhosis with the development of acquired por­
measured in a dog suspected or known to have hypoad­ tosystemic shunts. The underlying cause of hypoglyce­
renocorticism. A 2.5–5% dextrose infusion, usually mia results from inadequate amounts of functional liver
added to lactated Ringer’s or normal saline solution, tissue for optimal gluconeogenesis and glycogen storage
should be administered as soon as hypoglycemia is docu­ to maintain normal blood glucose levels.
mented in addition to glucocorticoid replacement ther­ The diagnosis of acquired liver dysfunction is usually
apy. If the pretreatment serum sodium and potassium quite straightforward. Common CBC, serum biochemi­
concentrations are normal, mineralocorticoid replace­ cal profile and urinalysis abnormalities may include
ment is not necessary over the short term, and may never microcytosis, low serum albumin, BUN and cholesterol
be indicated in some dogs with adrenal insufficiency concentrations, elevated serum bilirubin levels, elevated
(atypical hypoadrenocorticism). These dogs, despite low paired serum bile acid concentrations, ammonium biu­
serum aldosterone concentrations, are able to maintain rate crystals in the urine, radiographic evidence of abnor­
normal serum sodium and potassium levels for reasons mal liver size, and/or ultrasonographic changes consistent
that are unclear. with abnormal echotexture or liver size. A liver biopsy is