Page 512 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

CHAPTER • 20

Fluid Therapy in Endocrine and

Metabolic Disorders

David L. Panciera

Metabolicdisorderssuchascomplicateddiabetesmellitus, PATHOPHYSIOLOGY
hypoadrenocorticism, and heatstroke are associated with A combination of events must take place for ketoacidosis
marked disturbances in fluid homeostasis, electrolyte bal- to occur. Insulin deficiency, presence of counter-regu-
ance, and acid-base status. Prompt recognition of the latory hormones, fasting, and dehydration combine to
complications associated with these and other metabolic create the metabolic aberrations that result in the syn-
disorders is essential for effective management. The drome of DKA. 43 The insulin deficiency may be relative
dynamic nature of these illnesses during treatment or absolute. The diagnosis of diabetes mellitus is most
requires the attending clinician to be vigilant in monitor- often made at the time of presentation for DKA, but a
ing and to recognize when therapy needs to be altered. An minority of dogs and cats are receiving insulin at the time
understanding of the pathophysiology of the metabolic of diagnosis. The concurrent illness present in the major-
abnormalities encountered in each disorder is necessary ity of cases of DKA is the cause of insulin resistance and
for proper management. contributes to the increase in counter-regulatory
hormones.
DIABETIC KETOACIDOSIS
Carbohydrate Metabolism
Diabetic ketoacidosis (DKA) is a life-threatening compli- Hyperglycemia occurs as a result of insulin deficiency,
cation of diabetes mellitus that results from a combination increases in counter-regulatory hormones, and dehydra-
of factors,includinginsulinresistance(counter-regulatory tion. Increased hepatic glucose output primarily caused
hormones), fasting, alack ofinsulin, and dehydrationin an by increased gluconeogenesis appears to be the primary
animal with diabetes mellitus. Dehydration, electrolyte factor causing hyperglycemia. 18,43 Gluconeogenic
disturbances, and metabolic acidosis are consistent substrates include amino acids derived from proteolysis
findings in affected patients that must be addressed during and decreased protein synthesis, lactate from glycolysis,
treatment. Most animals with DKA have concurrent and glycerol from lipolysis. Increased glucagon and
diseases, including pancreatitis, urinary tract infection, b-adrenergic activation by catecholamines in the face of
hyperadrenocorticism, neoplasia, hepatic disease, and inadequate insulin stimulate glycolysis and gluconeogen-
renal failure. In addition to clinical signs typical of diabetes esis. The osmotic diuresis induced by glycosuria
mellitus,dogsandcatswithketoacidosisfrequentlyexhibit contributes to dehydration and subsequent hyperglyce-
lethargy, anorexia, vomiting, weakness, depression, dehy- mia. 18,43 Dehydration also may cause decreased insulin
dration, tachypnea, and weight loss. Other clinical signs delivery to sensitive tissues such as skeletal muscle and
may bepresent dependingonthe underlyingillness. Aten- therefore may reduce insulin action. In addition, antago-
tativediagnosisismadebydocumentingketonuriainadia- nism of the cellular actions of insulin by growth hormone
betic animal with clinical signs of systemic illness and and cortisol contribute to insulin resistance.
diabetesmellitus.Manydogswithuncomplicateddiabetes
mellitus will have ketonuria at the time of initial diagno- Lipid Metabolism
sis, 56 and it is important to distinguish ketosis that does Ketoacids are derived from the increased free fatty acids
not necessitate the aggressive treatment described below that are present as a consequence of increased lipolysis.
from dogs with true ketoacidosis. The prognosis more An increase in catecholamines results in activation of hor-
often is determined by the nature and severity of the con- mone-sensitive lipase in adipose tissue, liberating free
current disease than by the ketoacidotic state. fatty acids and glycerol. 18,43 In the liver, the large

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