Page 1360 - Clinical Small Animal Internal Medicine

1298 Section 11 Oncologic Disease

Diagnosis metastasis should be expected. Debulking of gross
VetBooks.ir Differential diagnosis for other causes of hypoglycemia disease may significantly assist in controlling clinical
signs. The goal of surgery is to remove as much neoplas­
include hypoadrenocorticism, juvenile hypoglycemia, sep­
sis, growth hormone deficiency, nonpancreatic tumors, tic tissue as possible. Special attention should be given to
insulin overdose, hepatic disease, glycogen storage diseases, regional lymph nodes and the liver. Complications
artifacts related to sample handling, and toxins. Other include hyperglycemia (diabetes mellitus), continued
types of neoplasms that can lead to paraneoplastic hypo­ hypoglycemia, exocrine pancreatic insufficiency, and
glycemia include hepatocellular carcinoma, hepatoma, pancreatitis.
leiomyosarcoma, leiomyoma, lymphoma, myeloma, and First‐line medical management is glucocorticoid ther­
hemangiosarcoma. apy. In particular, prednisone administered at 0.25–3 mg/
A minimum database (complete blood count, serum kg orally twice daily can be utilized. The dose should be
chemistry, urinalysis) should be collected to rule out increased as needed to control hypoglycemia. Prednisone
other causes of hypoglycemia. Nonspecific findings that is used with small frequent feedings (four times daily)
may be associated with insulinomas include elevated and limited exercise. Exercise leads to an increased
liver enzymes, hypokalemia, and hypophosphatemia. peripheral demand for glucose in spite of impaired glu­
Radiographs may help rule out other causes of hypoglyce­ coneogenesis and glycogenolysis. As a result, insulin
mia. However, radiographic changes directly related to secretion continues even as blood glucose falls.
insulinomas should not be expected. Sensitivity of identi­ Diazoxide decreases insulin release from beta‐cells
fying insulinomas with abdominal ultrasound can be as and stimulates epinephrine release from adrenergic cells.
low as 36%. It may be more beneficial in identifying metas­ The result is decreased insulin release and increased
tasis in the liver and local lymph nodes. Failure to identify hepatic glycogenolysis and gluconeogenesis. It is effec­
a pancreatic mass does not rule out an insulinoma. Serum tive in 64–85% of dogs. The recommended dose is 5 mg/
insulin concentrations that are normal to high in the pres­ kg every 12 hours but may be increased up to 30 mg/kg
ence of hypoglycemia support a diagnosis of insulinoma. every 12 hours if necessary. Thiazide diuretics potentiate
Insulin:glucose and glucose:insulin ratios have high false‐ the effects of diazoxide. The most common side‐effects
positive rates and are not recommended. Rather, insulin of diazoxide are gastrointestinal in nature.
concentration should be measured on a serum sample Octreotide is a somatostatin analog that activates
taken when the blood glucose is below 60 mg/dL. Insulin somatostatin receptors resulting in the inhibition of
concentrations should be low or undetectable at this blood synthesis and secretion of insulin. Octreotide is only
glucose concentration. The serum glucose and insulin are effective if the malignant beta‐cells are expressing soma­
evaluated as a pair. Animals may need to be fasted in order tostatin receptors (~60% in people). It is given at a start­
to obtain the appropriate samples and serial samples may ing dose of 2 μg/kg SC twice daily. The dose can be
need to be drawn every 2–4 hours until the blood glucose increased to three times daily. Limited studies suggest
concentration is below 60 mg/dL. Provocative testing is not that long‐term efficacy is poor. Side‐effects are limited
recommended as it has not been shown to be more sensi­ but the drug is costly.
tive than paired insulin and glucose measurement and can Streptozotocin is a chemotherapeutic agent that has
be dangerous due to potentiation of hypoglycemia. direct toxic effects on pancreatic beta‐cells. It is nephro­
Additional preoperative and intraoperative methods of toxic and therefore intravenous fluid diuresis is required.
tumor identification may be utilized. Nuclear scintigra­ It is administered once every 2–3 weeks at a dosage of
2
phy with indium 111‐labeled pentetreotide has been 500 mg/m for five treatments. If diabetes mellitus
used to image somatostatin receptors in dogs with insu­ occurs, treatment is discontinued. In one study on the
linomas. Insulinomas express high‐affinity somatostatin use of streptozotocin in dogs with insulinoma, controls
receptors of subtype sst2 (SST2), thus allowing abnormal lived for 90 days. Dogs had a median duration of normo­
foci of activity to be detected. Direct intraoperative glycemia of 163 days when given streptozotocin every
ultrasonography and intravenous injection of methylene three weeks. In another study, streptozotocin was given
blue may also be beneficial in identifying insulinomas. every two weeks and the average return of hypoglycemia
Methylene blue concentrates in the neoplastic tissue. was 196 days.
However, side‐effects including Heinz body anemia and
renal failure have been reported to occur. Prognosis
The World Health Organization (WHO) classification
Therapy
for tumor staging is prognostic for insulinomas. Factors
Surgery is the mainstay of treatment. However, even that affect prognosis include presence or absence of
when resectable, a cure is still unlikely. Gross or occult tumor (T0 or T1), regional nodal involvement (N0 or