Page 869 - Small Animal Internal Medicine, 6th Edition
P. 869

CHAPTER 49   Disorders of the Endocrine Pancreas   841


            dose of insulin, often occurring in conjunction with an infec-  on physical examination, and metabolic acidosis is mild (i.e.,
            tious, inflammatory, or insulin-resistant hormonal disorder.   with total venous carbon dioxide [CO 2 ] or arterial bicarbon-
  VetBooks.ir  Because of the close association between DKA and newly   ate concentration > 16 mEq/L), short-acting regular crystal-
                                                                 line insulin can be administered subcutaneously three times
            diagnosed diabetes mellitus, the signalment of DKA in dogs
            and cats is similar to that of nonketotic diabetics.
                                                                 therapy and intensive care usually are not needed. Because
              The history and physical examination findings are vari-  daily at 8-hour intervals until the ketonuria resolves. Fluid
            able, in part because of the progressive nature of the disorder   regular crystalline insulin is a potent insulin, the initial
            and the variable time between the onset of DKA and client   dosage (0.1-0.2 U/kg/injection) is lower than that recom-
            recognition of a problem. Polyuria, polydipsia, polyphagia,   mended for longer-acting insulin preparations. To minimize
            and weight loss develop initially but may be unnoticed or   hypoglycemia, the dog or cat should be fed one third of its
            considered  insignificant  by  the  client.  Systemic  signs  of   daily caloric intake at the time of each insulin injection.
            illness (e.g., lethargy, anorexia, vomiting) ensue as ketone-  Subsequent adjustments in the insulin dose are based on
            mia and metabolic acidosis develop and worsen, with the   clinical response and results of blood glucose measurements.
            severity of these signs directly related to the severity of the   Urine ketone concentrations should be monitored and, if
            metabolic acidosis and the nature of concurrent disorders   available, blood β-hydroxybutyrate concentrations should be
            that are often present. The time interval from onset of the   monitored using a portable glucose and ketone meter (e.g.,
            clinical signs of diabetes to development of systemic signs of   Precision Xtra®, Abbott). A decrease in the blood glucose
            DKA is unpredictable and ranges from a few days to several   concentration implies a decrease in ketone production. This,
            months. Once ketoacidosis begins to develop, however,   in combination with metabolism of ketones and loss of
            severe illness usually becomes evident within a week.  ketones in urine, will usually correct ketosis within 48 to 96
              Common physical examination findings include dehydra-  hours of initiating insulin therapy. Prolonged ketonemia and
            tion, lethargy, weakness, tachypnea, tachycardia, and some-  ketonuria is suggestive of a significant concurrent illness
            times a strong odor of acetone on the breath. Slow, deep   (e.g., chronic pancreatitis) or inadequate blood insulin con-
            breathing may be observed in animals with severe metabolic   centrations to suppress lipolysis and ketogenesis. Once the
            acidosis. Gastrointestinal tract signs such as vomiting and   ketosis has resolved, insulin therapy may be initiated using
            abdominal pain are common in animals with DKA, in part   longer-acting insulin preparations. As a general rule of
            because of the common concurrent occurrence of pancreati-  thumb, the initial dosage of the longer-acting insulin prepa-
            tis.  Other  intraabdominal disorders should  be  considered   ration is approximately the same as the dosage of regular
            and diagnostic tests (e.g., abdominal ultrasound) performed   crystalline insulin administered at the time the switch in
            to help identify the cause of the gastrointestinal signs. Addi-  insulin is made, with subsequent adjustments in the dosage
            tional physical examination findings associated with uncom-  based on the animal’s response to the insulin.
            plicated diabetes mellitus (e.g., hepatomegaly, cataracts,
            diabetic neuropathy) may be identified.              Treatment of Sick Dogs or Cats With
                                                                 Diabetic Ketoacidosis
            Diagnosis                                            Aggressive therapy is called for if the dog or cat has systemic
            The diagnosis of diabetes mellitus is based on appropri-  signs of illness (e.g., lethargy, anorexia, vomiting); physical
            ate clinical signs, persistent fasting hyperglycemia, and   examination reveals dehydration, depression, weakness, or a
            glycosuria. The concurrent documentation of ketonuria   combination of these; or metabolic acidosis is severe (i.e.,
            establishes a diagnosis of DK and documenting metabolic   total venous CO 2  or arterial bicarbonate concentration  <
            acidosis establishes the diagnosis of DKA. Commonly   12 mEq/L). The five goals of treatment of a severely ill, keto-
            used nitroprusside reagent test strips for ketonuria (e.g.,   acidotic, diabetic pet are (1) to provide adequate amounts of
            KetoDiastix) measure only acetoacetate and its byproduct   insulin to suppress lipolysis, ketogenesis, and hepatic gluco-
            acetone. β-hydroxybutyrate is not detected by conventional   neogenesis; (2) to restore water and electrolyte losses; (3) to
            nitroprusside tests. If ketonuria is not present but DKA is   correct acidosis; (4) to identify the factors precipitating the
            suspected, serum or urine can be tested for acetone using   present illness; and (5) to provide a carbohydrate substrate
            Acetest tablets, blood can be tested for the presence of   (i.e., dextrose) when necessary to allow continued adminis-
            β-hydroxybutyrate using a quantitative enzymatic assay or   tration of insulin without causing hypoglycemia (Box 49.11).
            a portable blood glucose and ketone analyzer (e.g., Preci-  Proper therapy does not mean forcing a return to a normal
            sion Xtra, Abbott Diagnostics), or plasma from heparinized   state as rapidly as possible. Because osmotic and biochemical
            hematocrit tubes can be used to test for the presence of   problems can arise as a result of overly aggressive therapy as
            acetoacetate using urine reagent test strips used to docu-  well as from the disease itself, rapid changes in various vital
            ment ketonuria.                                      parameters can be as harmful as, or more harmful than, no
                                                                 change. If all abnormal parameters can be slowly returned
            Treatment of “Healthy” Dogs or Cats With             toward normal over a period of 24 to 48 hours, therapy is
            Diabetic Ketosis or Diabetic Ketoacidosis            more likely to be successful.
            If systemic signs of illness are absent or mild, inappetence is   Critically important information for formulating the
            not present, serious abnormalities are not readily identifiable   initial treatment protocol includes hematocrit and total
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