An Uncontrolled Diabetic Dog

Ann Della Maggiore, DVM, DACVIM, serves as an adjunct professor of clinical internal medicate at the University of California, Davis School of Veterinary Medicine, with a specific pastime in small animal endocrinology. She received her veterinary degree from UC Davis, then completed a residency in belittled animal home medicine at the same institution. Evaluating a ill controlled diabetic pet can be frustrating for both the clinician and the owner. The veterinarian must conduct a exhaustive examination of the patient, along with careful monitor, to successfully stabilize these animals. There are critical questions that must be answered .

Questions: Investigating the Unstable Diabetic Dog

1. What are possible causes of poor diabetic control in this dog?
2. Are there problems with insulin handling and administration?
3. Is this dog receiving an appropriate insulin type and dose?
4. What and when is the dog being fed, and does the dog receive any additional treats or table scraps?
5. What are possible causes of insulin resistance in this dog?
6. What additional diagnostics would help in better assessing diabetic control?

Buster, a 7-year-old male castrated beagle mix weighing 18 kilogram, was presented for evaluation of uncontrolled diabetes .

History

Previous Diagnosis

Six months before display, Buster was presented to his primary veterinarian for polyuria, polydipsia, and weight passing. physical examination and complete blood consider ( CBC ) were everyday, while the serum biochemical profile ( Table 1 ) demonstrated :

Reading: An Uncontrolled Diabetic Dog

• Mildly increased alkaline phosphatase (ALP)
• Mild hypercholesterolemia
• Hyperglycemia

The urinalysis showed glucosuria, with no attest of ketones, white blood cells, or bacteria. Based on these findings, Buster was diagnosed with diabetes mellitus .

Medical Therapy

After diagnosis, Buster ’ s primary veterinarian initiated therapy with neutral protamine Hagedorn ( NPH ) insulin at 9 U ( 0.5 U/kg ) SC q12h. Intermittent touch rake glucose monitor was used to determine adjustments in insulin dose and, based on variably high results ( > 350 mg/dL ), Buster ’ s insulin venereal disease was increased approximately every 3 days .
Upon presentation for a second gear opinion on diabetic control, Buster was receiving 30 U of NPH insulin q12h. The insulin was from a fresh prescription, stored in the refrigerator, and the administration technique ( visualized as separate of history collection ) appeared appropriate. Buster had no other known medical conditions and was not receiving any other drugs or supplements .

Diet & Exercise

Buster was receiving a care diet ( day by day requirements calculated at 700 calories/day ; he was receiving approximately 800 calories/day ), divided and fed in equal amounts approximately 10 to 12 hours apart. The diet and exert convention had been consistent since diagnosis .

Unstable Diabetic Dog: History and Physical Examination

A thorough history is key, including probe into both the animal ’ s general history and specific questions related to diabetic history, such as initial diagnosis and management. When possible, available medical records should besides be thoroughly reviewed .
key points to any diabetic animal ’ south history include the following1,2 :

Clinical Signs

The owners noted that Buster was polyphagic, polyuric, and polydipsic, with no obvious improvement since knowledgeability of insulin therapy. Buster had no holocene vomit, diarrhea, or alterations in appetite .

Physical Examination

physical interrogation revealed a symmetrically muscled chase with mild muscle atrophy, with a body condition grudge of 7/9. Buster had control periodontic disease, a grade III/VI left apical systolic heart murmur, incomplete bilateral diabetic cataracts, and a tense, nonpainful abdomen on palpation. No extra abnormalities were appreciated .

Unstable Diabetic Dog: Diagnostic Approach

For a patient with uncontrolled diabetes mellitus, the goal of the diagnostic evaluation is to establish a problem list of conditions relate and unrelated to the animal ’ sulfur diabetes mellitus .
In addition, determine the suspected causes of poor diabetic control, which may include :

• Problems with owner administration
• Activity of the insulin
• Insulin overdose or underdose
• Prolonged or short duration of insulin effect
• Concurrent disease causing insulin resistance

Diagnostic Approach

Buster ’ randomness problem tilt of conditions—both related and unrelated to his diabetes mellitus—included :

• Poorly controlled diabetes mellitus
• Bilateral incomplete diabetic cataracts
• Grade III/VI systolic heart murmur
• Periodontal disease

distrust causes of inadequate diabetic command included :

• Insulin overdose
• Inappropriate insulin type (eg, short duration of action)
• Insulin resistance caused by concurrent disease

Initial Laboratory Analysis

Routine CBC, serum biochemical profile, and urinalysis with urine culture were performed. The CBC was everyday and urine acculturation was negative for bacterial emergence. The primary abnormalities noted on the serum biochemical visibility were elevated ALP, hypercholesterolemia, and hyperglycemia ( Table 2 ) .

Glucose Monitoring and Curves

The patient was hospitalized in ordain to better assess diabetic dominance through serial blood glucose curves and monitor .
Day 1: Blood glucose was assessed in-hospital on the night of admission ( Table 3 ), before insulin government .

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Day 2: Blood glucose monitor began the adjacent dawn ( Table 3 ). Because blood glucose was lower than anticipated at 8 am, Buster received 25 U of NPH insulin SC after a complete meal, with blood glucose measurements taken 2 hours later and then q2h .
Buster importantly responded to insulin while in the hospital, with a relatively first gear rake glucose at 8 phase modulation. Buster was fed and no extra insulin was administered on Day 2. Blood glucose monitor continued nightlong until lineage glucose was > 200 mg/dL .
Day 3: Buster received 10 U of NPH insulin SC after a complete meal in the morning, with reception monitored throughout the day ( Table 3 ) .
Figure 1 depicts the blood glucose measurement trends revealed over the 3 days of in-hospital monitor .

Blood Glucose Curves

Blood glucose concentrations can vary significantly in diabetic animals. Blood glucose curves can, consequently, provide more utilitarian impressions of how diabetic animals respond to insulin administration than individual measurements entirely .
coincident monitoring of body weight unit, clinical signs ( water system pulmonary tuberculosis, micturition, appetite ), and fructosamine measurements should accompany blood glucose monitor, as rake glucose curves are well evaluated with this extra information in handwriting .
key questions to ask when evaluating blood glucose curves include :

1. Is the insulin effective at decreasing the blood glucose? If ineffective, consider insulin underdose, overdose causing rebound hyperglycemia or Somogyi response, or insulin resistance. It is also important to review the animal’s history and physical examination findings to help prioritize possible causes of poor diabetic control.
2. What is the nadir? If the nadir is too high or too low, consider an insulin dose that alternates.
3. What is the duration of action of the insulin? If too short or too long, consider changing the insulin type.

Clinicians must recognize the variability between blood glucose curves performed at home and those obtained in the hospital setting. many owners may alter a pet ’ s daily routine ( eg, feed schedule, drill ) to accommodate the hospital visit. In accession, pets exhibiting fear or stress in a hospital set are improbable to be good candidates for in-hospital blood glucose curves. At-home rake glucose monitor or other approaches ( for exercise, continuous glucose monitors ) must be considered .

Diagnosis and Therapy

On the basis of serial rake glucose curves and monitoring in the hospital, it was suspected that Buster was exhibiting clinical signs reproducible with hapless control caused by rebound hyperglycemia, besides known as the Somogyi response .
This diagnosis was based on Buster ’ s clinical response ( deoxidize clinical signs and increased torso system of weights ) and improved blood glucose values, both of which were associated with a meaning decrease in insulin dose. See The Somogyi Response for further details on diagnosis of rebound hyperglycemia .

Challenges in Diagnosis

The particular criteria for a Somogyi reception were not demonstrated on Buster ’ s rake glucose curves performed in the hospital. however, these criteria can be challenging to identify in hospital, and may not be identified at all because of :

• Infrequent sampling in the hospital
• The fact that diabetogenic hormones released during the response can have lingering effects—up to 24 to 72 hours following the period of hypoglycemia
• Increased stress caused by hospitalization

According to the blood glucose values obtained in hospital for Buster, once the insulin venereal disease was reduced significantly, Buster ’ s blood glucose values improved, leading to suspicion of insulin overdose .

Definitive Diagnosis

In this frump, if the previous high insulin dose had been administered repeatedly, a Somogyi reaction with rebound hyperglycemia may have been documented in subsequent blood glucose curves .

Treatment and Follow-up

Buster ’ s Day 3 dose of NPH insulin ( 10 U SC q12h ) was continued for 7 to 10 days, with a design for the owner to return with Buster in 1 week for a blood glucose curve .
At Buster ’ s follow-up appointment, his clinical signs had improved but not resolved. A blood glucose curve was performed, revealing a nadir of 260 mg/dL at 4 promethium. The insulin was effective, but the nadir was not ideal. therefore, the dose was increased to 12 U of NPH insulin SC q12h .
extra follow-up showed that, with this dose, Buster ’ s clinical signs had resolved and his condition was controlled .

The Somogyi Response

The Somogyi reception, besides called rally hyperglycemia and insulin-induced hyperglycemia, is the physiologic reaction to impending hypoglycemia. This reaction is characterized by foreplay of liverwort gluconeogenesis and secretion of diabetogenic hormones, including catecholamines and glucagon .

Incidence & Risk Factors

limited literature supports the documentation of the Somogyi reaction in dogs and cats. A holocene study suggests that, in cats receiving long-acting insulin analogs ( eg, insulin glargine, insulin detemir ), the Somogyi reply is less park than initially suspected.3
Factors that may increase risk for the Somogyi response in dogs and cats include :

• Insulin adjustments made very frequently, which does not give the patient time to equilibrate between doses
• Insulin adjustments made in large increments
• Lente insulin therapy q12h.

Clinical Signs

clinical signs of hypoglycemia are often elusive and overshadowed by signs of hyperglycemia that go unnoticed by the client.1,2,4 Table 4 provides a list of common clinical signs of hyperglycemia and hypoglycemia .

Diagnosis

diagnosis of the Somogyi answer requires documentation of hypoglycemia (glucose <65 mg/dL) followed by hyperglycemia (glucose >300 mg/dL) after insulin administration.
Rebound hyperglycemia is frequently between 400 and 800mg/dL. It is suspected that patients exhibit prolong hyperglycemia and insulin resistance ( up to 24–72 H ) after a hypoglycemic event.1,2,4
The Somogyi answer should be suspected when :

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• Blood glucose rapidly drops regardless of nadir.
• Duration of insulin is greater than 12 hours.
• The patient is receiving a high dose of insulin (>1.5 U/kg).
• There is a cyclic history of good glycemic control for 1 to 2 days, followed by poor glycemic control for several days.
• The patient has gained weight despite suboptimal diabetic control.
• The patient has failed to improve despite increasing the insulin dose.

Challenges With Recognition

respective challenges surround diagnosis of a Somogyi response. The Somogyi response :

• Is rare in dogs and cats. Previously believed to be more common in cats on lente insulins. Perceived to be less common in feline patients receiving new analog insulin preparations, although there is limited literature describing prevalence in diabetic animals.1,2,4
• Does not happen in every episode of hypoglycemia. Reasons for this are unclear, but may include lack of a counterregulatory hormone response and duration of hypoglycemia.
• Can be challenging to detect with blood glucose curves because the period of hypoglycemia can be very short and easily missed.
• Is associated with unpredictable serum fructosamine measurements. Usually, a concentration greater than 500 mcmol/L confirms poor diabetic control.1,2,4

Because of these challenges, when insulin overdose is suspected, but not documented on a blood glucose arch, consider reducing the insulin dose. Once the dose has been reduced, instruct the owner to carefully monitor clinical signs for any elusive change and recur monitor at least 4 to 7 days after reducing the insulin dose.1,2,4

Summary

mentally ill diabetic animals can be a contend to manage in clinical rehearse. Thorough communication with the owner and interrogation of the animal, along with careful monitor, are the key to successfully stabilizing these animals. Making minor, infrequent insulin dose changes and allowing clock to assess the animal ’ sulfur response are the best ways to prevent insulin overdose .

Answers: Investigating the Unstable Diabetic Dog

1. What are possible causes of poor diabetic control in this dog? Insulin overdose, inappropriate insulin type, insulin resistance caused by concurrent disease.
2. Are there problems with insulin handling and administration? Not in this case.
3. Is this dog receiving an appropriate insulin type and dose? Insulin dose is too high and does not provide good diabetic control; the insulin type should be appropriate, but duration of action cannot be assessed currently.
4. What and when is the dog being fed, and does the dog receive any additional treats or table scraps? Appropriate caloric intake is provided twice daily, with no treats or table scraps.
5. What are possible causes of insulin resistance in this dog? Hyperadrenocorticism, hypertriglyceridemia, insulin antibodies, periodontal disease, or other concurrent disease.
6. What additional diagnostics would help in better assessing diabetic control? Blood glucose curve (performed in hospital or at home), fructosamine concentration; further diagnostics can be based on findings and may include systemic evaluation for concurrent disease or continuous glucose monitoring, if available.

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