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Abstract

Objectives

The purpose of this study was to review the characteristics of diabetic cats presenting to a specialty and emergency center for signs attributed to hypoglycemia and to identify the factors that may have contributed to the hypoglycemic episode, the patient’s clinical signs and laboratory findings, and the response of hypoglycemic cats to therapy.

Methods

Twenty-eight cats were presented a total of 30 times for symptomatic hypoglycemia. Data were collected from cat owners at the time of presentation and from subsequent patient records.

Results

The majority of cats presented for neurologic signs attributed to the reduced ingestion or subsequent vomiting of a meal after insulin had been administered or the accidental double-dosing of insulin. Concurrent illnesses that may have affected insulin requirements were also common.

Conclusions and relevance

Cats that demonstrated clinical improvement within 12 h of treatment were more likely to recover despite their mental status and glucose level on presentation.

Introduction

Hypoglycemia is one of the most common adverse events associated with insulin therapy in humans with diabetes mellitus. Symptomatic hypoglycemia requiring treatment has been reported to occur in up to 40% of individuals receiving insulin each year,^1–3 accounting for >97,000 annual emergency room visits.⁴ In a cohort study of 23,752 humans with insulin-treated diabetes diagnosed under the age of 30 years, 18% of male deaths and 6% of female deaths were attributed to hypoglycemia.⁵

Hypoglycemia is also a significant concern when pursuing insulin therapy in cats with diabetes mellitus. In a quality-of-life study, >50% of diabetic cat owners worried that a hypoglycemic episode might occur and 35% of owners indicated hypoglycemic episodes could possibly be occurring in their cats.⁶ Recent International Society of Feline Medicine consensus guidelines on feline diabetes mellitus recommend prioritizing avoidance of hypoglycemia at the expense of allowing periods of hyperglycemia.⁷

Investigational studies of diabetic cats, in which blood glucose curves were being performed to evaluate insulin treatment protocols, indicate that hypoglycemia is common. Low blood glucose readings were reported in 21/67 cats receiving treatment with protamine zinc insulin, whereas clinical signs of hypoglycemia developed in five of these cats.⁸ Another study evaluating protamine zinc insulin treatment in 133 cats identified asymptomatic hypoglycemia in blood glucose curves performed in 64% of the cats.⁹ In a study comparing diabetic control in cats receiving lente, protamine zinc or glargine insulin, asymptomatic hypoglycemia on blood glucose curves was reported to be ‘common’, whereas clinical signs of hypoglycemia were reported in 3/24 cats.¹⁰ Meanwhile, at least one episode of hypoglycemia was identified in 93% of 55 cats that underwent an intensive treatment protocol utilizing glargine insulin and dietary management.¹¹ Asymptomatic hypoglycemia has also been reported in cats being treated with detemir insulin.¹²

The clinical signs, treatment and outcomes of diabetic cats presenting to a specialty and emergency center for hypoglycemia have not been well documented. The characteristics of insulin-induced hypoglycemia in 20 client-owned diabetic cats presenting to a university referral hospital were reported for the period 1986–1993.¹³ Recommendations for treating diabetes mellitus in cats have significantly changed since 1993 as have the types of insulin now available. Protamine zinc, glargine and detemir insulins are now recommended owing to their slower absorption characteristics and longer duration of action. Twice-daily dosing has also become the standard treatment regimen in addition to dietary modification. Many clinicians are pursuing more intensive treatment protocols with the goal of inducing diabetic remissions.^10–12

The purpose of this study was to review the characteristics of diabetic cats receiving insulin therapy presenting to a specialty and emergency center for clinical signs attributed to hypoglycemia and to identify the factors that may have contributed to the hypoglycemic episode, the patient’s clinical signs and laboratory findings, and the response of hypoglycemic cats to therapy.

Material and methods

Criteria for case selection

From 1 March 2013 to 1 December 2015, records from cats receiving insulin therapy to treat diabetes mellitus presenting to BluePearl Veterinary Partners in Kansas City for clinical signs of hypoglycemia confirmed by blood testing were evaluated. Hypoglycemia was defined as a blood glucose <65 mg/dl (<3.6 mmol/l).

Data collected prospectively at the time of presentation included sex, breed, age and weight. In addition, duration of insulin treatment, frequency of insulin administration, the insulin type and dose, at-home monitoring being performed and any recent changes in insulin dosage were recorded. Information was also collected regarding previously diagnosed hypoglycemic events in the patient, pre-existing illness, the specific clinical signs noted at home responsible for the patient’s presentation and the owners’ perception as to why this event may have occurred.

Laboratory testing and treatments were performed at the discretion of the clinician evaluating the patient. Blood glucose measurements were performed utilizing a hand-held portable veterinary glucose monitor calibrated for cats. ‘Low’ blood glucometer readings (<20 mg/dl [<1.1 mmol/l] according to the glucometer manufacturer) were duly noted. Results of blood work, urinalysis, urine cultures, thoracic radiographs and ultrasound examinations were recorded. Results of physical and neurologic examinations performed at presentation, 12 h post-presentation, 24 h post-presentation and at each subsequent 24 h period the patient remained hospitalized, as well as patient outcomes were noted. Follow-up calls were performed with the owners of discharged patients and/or their primary veterinarians to determine their post-discharge recovery status.

For evaluation of treatment outcomes, cats were divided into those presenting with neurologic signs of (1) mentally dull, weak and/or ataxic but responsive; or (2) stupor or coma. The outcomes for cats with ‘low’ blood glucometer readings on presentation were also noted as a separate group.

Results

Twenty-eight cats receiving insulin therapy to treat diabetes mellitus were presented between 1 March 2013 and 1 December 2015 for clinical signs attributable to hypoglycemia. Two of these cats presented twice during the study period for a total of 30 presentations.

Signalment

The population of 28 cats was comprised of 17 castrated males, one intact male and 10 spayed females. Twenty cats were domestic shorthairs, two were domestic longhairs, two were domestic mediumhairs, two were Maine Coons, one was Siamese and one was a Russian Blue. Median age of the 28 cats was 13 years (range 3–19 years). Median weight was 6.0 kg (range 2.2–10.5 kg). Fifteen of the 28 cats weighed >6.0 kg and were considered to be obese.

Insulin therapy on presentation

Upon presentation, 13 cats were being treated with glargine insulin, 10 cats were being treated with protamine zinc insulin, six cats were receiving neutral protamine hagedorn (NPH) insulin, and one cat was receiving porcine insulin zinc (Table 1). One cat receiving glargine insulin and one cat receiving protamine zinc insulin presented twice during the study period. All of the cats were being dosed with insulin twice daily.

Table 1

Neurologic status on presentation

	Coma–stupor	Dull, weak and/or ataxia	Normal
Number of presentations	15	14	1
Insulin type
Glargine	6	6	1
Protamine zinc	6	4
NPH	3	3
Porcine insulin zinc		1
Duration of insulin treatment
<6 months	7	2
6 months to 1 year	1	3
>1 year	7	9	1
Blood glucose on presentation*
‘Low’ (<20 mg/dl; <1.1 mmol/l)	10	4
>20 mg/dl (median; range)	5 (29; 22–42)	10 (29; 21–48)	1 (38)
Improvement by
<12 h	9	13	1
Outcome
Recovered	9	13	1
Euthanized	6	1
Time to euthanasia post-presentation
<12 h	2
12–24 h	2
24–48 h	1	1
48–96 h	1
Insulin dose (U/kg body weight)
<1 U/kg	10	8	1
1.01–1.49 U/kg	4	5
>1.5 U/kg	1	1

AlphaTRAK 2 glucometer (Zoetis) provides a reading of ‘low’ for glucose <20 mg/dl

NPH = neutral protamine hagedorn

The median insulin dose per injection per cat for the 30 presentations was 0.8 units (U)/kg body weight (range 0.2–1.8 U/kg body weight). Seven cats (23%) had had their insulin dose increased within 3 months of their initial presentation, whereas three cats (10%) had had their dose decreased. In the two cats presented a second time during the study period, their insulin dose had been decreased from an average 1.2 U/kg body weight to 0.6 U/kg body weight per dose prior to the second presentation.

The duration of insulin therapy in cats presenting with hypoglycemia ranged from <1 month to 10 years. Nine out of 30 cats (30%) had been receiving insulin therapy for <6 months. An additional four cats (13%) had been receiving insulin treatment for <1 year. Seventeen out of 30 cats (57%) had been receiving insulin therapy for >1 year. Of the two cats presented a second time during the study period, one cat had been receiving insulin therapy for <6 months, whereas the other cat had been receiving insulin for >1 year.

History

Six out of 28 cats (21%) were reported to have been treated for a previous hypoglycemic reaction prior to the study period. Ten out of 28 cats (36%) were reported to have a concurrent medical condition. Three cats were reported to have arthritis and one cat each was reported to have inflammatory bowel disease, hypertension, chronic conjunctivitis and sinusitis, recurrent constipation, hyperthyroidism, crystalluria and intermittent vomiting. Four cats had been receiving treatment with medications other than insulin including prednisone, robenacoxib, meloxicam and clopidogrel.

A cause for the hypoglycemic episode was suspected by owners in 16/30 (53%) presentations. Ten owners believed their cat had not eaten as much food as normal on the day of presentation, one of which had also vomited; three owners indicated their cat had vomited despite eating normally; and three owners confirmed that their cat had been double-dosed with insulin.

Signs on presentation

The most common clinical signs reported by owners in their cats at home on the day of presentation were an inability to walk (n = 12), lethargy (n = 11), weakness (n = 11), failure to respond to stimulus (n = 10), twitching (n = 10), vocalizing (n = 6), ataxia (n = 5), seizure (n = 4), vomiting (n = 4), panting (n = 3), decreased appetite (n = 2), inappropriate urination (n = 2), diarrhea (n = 1) and drooling (n = 1).

Neurologic signs were noted on initial physical examination in 29/30 presentations (Table 1). Fourteen cats (47%) were considered mentally dull, weak and/or ataxic but responsive. Six out of 14 cats were non-visual. Excessive vocalization was noted in 5/14 cats. Fifteen cats (50%) presented in a state of stupor or coma, responding only to intensive stimuli or not at all. None of these 15 cats were considered visually responsive. One of these cats was seizuring when first examined. One of the 30 cats, which had presented for lethargy, was reportedly normal on initial physical examination. Non-neurologic signs noted on initial physical examination in the 30 cats included bradycardia (n = 5), hypothermia (n = 3), panting (n = 2) and hyperthermia (n = 1). A small skin laceration was identified in one cat.

Diagnostic findings

The blood glucose concentration at presentation was <65 mg/dl (<3.6 mmol/l) in all of the cats. Ten out of 15 cats (67%) presenting with coma/stupor had ‘low’ glucometer readings, whereas 4/14 cats (29%) presenting with mental dullness, weakness and/or ataxia had ‘low’ glucometer readings. Blood glucose values in the remainder of the cats varied between 21 and 51 mg/dl (1.2–2.8 mmol/l). The blood glucose in the one physically normal cat that had presented for lethargy was 38 mg/dl (2.1 mmol/l).

Complete blood cell counts and serum chemistry profiles were performed in 19 cats. Hypokalemia (normal potassium levels were considered to be between 3.6 and 5.5 mEq/l) was the most common abnormality noted in 8/19 cats. Additional abnormalities included elevated blood urea nitrogen (n = 5), elevated creatine phosphokinase (n = 3), leukocytosis with a neutrophilia (n = 3), elevated alanine aminotransferase (n = 3), elevated creatinine (n = 2), leukopenia (n = 1), hyperglobulinemia (n = 1), hypercholesterolemia (n = 1) and anemia (n = 1). A urinalysis was performed in 13 cats. Abnormal urinalysis results included pyuria (n = 3), proteinuria (n = 7), glucosuria (n = 4), hematuria (n = 4) and bacteriuria (n = 1). Only one cat had a urine culture performed (not the cat with bacteriuria) and it showed no growth. Abdominal ultrasound was performed in 7/30 cats. Abnormalities included hepatic nodules (hepatic cytology showed mild hydropic degeneration; n = 1), hypoechoic pancreas (n = 2), left adrenal mass (n = 1) and ascites (n = 1). Echocardiography demonstrated hypertrophic cardiomyopathy in one cat.

Treatment and outcomes

All cats were hospitalized for treatment. Treatments varied according to the clinician overseeing the patient. All cats were administered intravenous (IV) dextrose boluses, varying from 1.5–6 ml of 25% and 2–4 ml of 50% dextrose on presentation followed by IV fluids supplemented with dextrose. Dextrose supplementation in the IV fluids varied between 2.5% and 5%. Hypoglycemia had resolved in all cats within 4 days of presentation (range 5 mins–4 days). Eighteen/30 cats (60%) had resolution of their hypoglycemia within 2 h. Subsequent blood glucose measurements in 6/30 cats (20%) was >300 mg/dl (>16.7 mmol/l) for varying periods of time as a result of treatment. Additional treatments included diazepam, mannitol, dexamethasone, thiamine, phenobarbital, levetiracetam, antiemetics and antibiotics. Food was offered to all cats when deemed alert enough to eat.

Treatment outcomes are noted in Table 1. Within 12 h of presentation, 13/14 cats (93%) presenting with mental dullness, weakness and/or ataxia had demonstrated neurologic improvement. One cat failed to show neurologic improvement and was humanely euthanized within 12 h of presentation. Ten/14 cats remained hospitalized, whereas 3/14 cats transferred to their primary care veterinarian for ongoing care. By 48 h after presentation, 13/14 cats (93%) were reported to be clinically normal. Five/6 cats that were assessed as being non-visual on presentation regained their vision within 48 h of presentation, whereas the sixth non-visual cat was euthanized at our facility owing to failure to show neurologic improvement.

At 12 h after presentation, 7/15 cats presenting with stupor or coma were responsive and ambulatory. Two cats had improved but were still considered mentally dull and weak. Four cats continued to be non-responsive and recumbent. Two cats had been euthanized within 12 h of presentation owing to an unchanging neurologic status, despite resolution of their hypoglycemia. Facial tremors/seizures had developed in two cats, one of which had become responsive. At 24 h after presentation, both of the improved cats (that were mentally dull and weak at 12 h) were considered to have completely recovered. Two additional cats presenting with stupor or coma had been euthanized owing to an unchanging neurologic status and in one of these cats the additional identification of ascites of undetermined origin. Two cats continued to be non-responsive and recumbent, both of which were ultimately euthanized (one at 48 h after presentation and one at 96 h after presentation) for an unchanging neurologic status. Nine of the 15 cats presenting in a state of stupor or coma that had improved within 12 h of presentation were discharged to their owners within 96 h of presentation. Three of the discharged cats had not regained their vision at the time of discharge. These cats were later reported by owners to have regained their vision within a few days of discharge. Six out of 15 cats, all of which had not improved within 12 h after initiating treatment, were ultimately euthanized for unchanging neurologic status.

Necropsies were not performed on any of the euthanized cats.

At 12 h after presentation, the single cat that was considered normal on physical examination was discharged to its owner.

Discussion

For clinical purposes several different glucose values have been used to define hypoglycemia in both the human and veterinary literature. A blood glucose value <65 mg/dl (<3.6 mmol/l) was chosen as the cut-off for classifying cats as hypoglycemic in this study as it approximates the glycemic threshold for activation of the glucose counter-regulatory systems in non-diabetic humans and the upper limit of blood glucose level reported to reduce counter-regulatory responses to subsequent hypoglycemia.^14,15 The 65 mg/dl value also approximates the upper limit of the cut-off for hypoglycemia used by the American Diabetes Association and the Endocrine Society,¹⁶ and was used to define hypoglycemia in a previous study evaluating insulin overdose in dogs and cats.¹³

The signalment of diabetic cats presenting for hypoglycemia in this study was similar to that previously reported in hypoglycemic cats and likely represents those cats at greatest risk for developing diabetes mellitus.^13,17,18 The median weight (6.0 kg) of cats in this study was similar to that reported in a previous study in which hypoglycemic cats had a median weight of 5.8 kg. Information was not available to determine if the cats presenting for hypoglycemia in this study weighed more than our hospital’s feline diabetic population as has been previously reported.¹³ Obesity is a risk factor for the development of feline diabetes mellitus. Weight loss could predispose diabetic cats to hypoglycemia by reducing their insulin requirement.¹⁹ It is unknown whether any of the cats in this study had lost weight in the period leading up to their hypoglycemic episode.

Similar to a previous report, hypokalemia was the most common laboratory abnormality identified in hypoglycemic cats in this study.¹³ The hypokalemia is likely secondary to the mobilization of potassium into the cells of the liver and musculature caused by the excessive dose of insulin.²⁰ Diminished dietary intake of potassium could also have contributed to the low potassium levels.

The cause for hypoglycemia was suspected in 16/30 presentations and included the reduced ingestion or subsequent vomiting of a meal after insulin had been administered and the accidental double-dosing of the insulin. In the remainder of the presentations, the reason for hypoglycemia was unknown. Concurrent illnesses are common in diabetic cats and can serve as a potential cause for changing insulin requirements.^9,11,18,21 Concurrent illnesses were communicated by owners in 10 of the cats, whereas diagnostic testing identified concurrent abnormalities in five cats, including cardiomyopathy, adrenal tumor, urinary tract infection and ascites. A number of abnormalities identified on blood work, which were not investigated further, would also suggest the presence of additional cats with complicating conditions. Periods of insulin resistance secondary to concurrent inflammatory disorders, as well as metabolic disorders that might affect the cat’s daily appetite, may oscillate day by day in severity. Insulin requirements may have been reduced on the day of the hypoglycemic episode in some of these cats.

In this study, glargine was the most common insulin type used in cats, followed closely by protamine zinc and then NPH-type insulins. Insulin dosing was being performed twice daily in all cats. Not knowing the prevalence of each insulin type’s use in our general population of diabetic cats makes it difficult to know if one insulin type or another is more likely to induce hypoglycemia. Glargine insulin use in people with type 1 and type 2 diabetes mellitus has been associated with a decreased incidence of hypoglycemic events.^22–25 To date, studies have failed to prove whether one insulin type is more likely to induce diabetic remission than other insulin types.²⁶ Feline studies evaluating insulin therapy protocols utilizing glargine indicate that hypoglycemia is common but that clinical signs are infrequent.^10,11 If an insulin were more likely to induce diabetic remission, its use would be expected to be associated with an increased incidence of hypoglycemic events unless intensive glucose monitoring and insulin dose adjustments were being performed.

Diabetic remissions have been reported to most commonly occur within 6 months of starting insulin therapy.^10–12,21 Eight cats in this study had been receiving insulin therapy for <6 months, although one of these cats was known to have been double-dosed with insulin. Reduced insulin requirements in feline diabetics have been attributed to the reversal of glucose toxicity, as well as resolution of concurrent illnesses which may have antagonized insulin action.^10,27,28 Even if remission was not achieved the insulin requirements of the cats in this study could have decreased. Long-term follow-up had not been performed in any of the cats in this study to determine if their subsequent maintenance insulin requirements decreased or if their diabetes resolved.

Multiple cats in this study experienced multiple hypoglycemic events. Two cats presented a second time during the study period for hypoglycemia, whereas six cats were reported by their owners to have required treatment for hypoglycemia prior to the study. Both cats presenting twice during the study period had had their insulin dose decreased prior to their second hypoglycemic episode. Further evaluation of the adequacy of their insulin dosing had not been performed prior to their second presentation. Decreasing insulin requirements due to reversal of complicating illnesses or glucose toxicity could have predisposed these cats to repeat hypoglycemic episodes. Impairment of hypoglycemic-induced counter-regulatory mechanisms could also have contributed to repeat hypoglycemic episodes. Studies in humans and rodents have suggested that the occurrence of hypoglycemic episodes predisposes them to future episodes.^29–35 Lower blood glucose levels must be reached before a compensatory counter-regulatory response is triggered, increasing the individual’s risk for symptomatic hypoglycemic episodes.^34,36 This delay in the compensatory response has been partially attributed to defects in the release of epinephrine and a reduction in the hepatic response to epinephrine.^33,37,38 In the absence of sympathetic nervous system stimulation and its associated signs, there is a reduced awareness in human diabetics that a hypoglycemic episode is occurring, termed ‘hypoglycemia unawareness’.^34,39 Affected individuals fail to develop symptoms that would prompt them to seek glycemic support prior to the development of more severe signs. Whether cats are similarly unaware of a dropping blood glucose level, which might otherwise trigger them to eat more food, is unknown. Failing to demonstrate signs of sympathetic stimulation, owners of these cats would not be aware that their cat’s blood glucose level had dropped until the more severe signs of neurologic dysfunction became evident. It is important that cats are monitored closely after insulin dosage changes given the potentially subtle signs of hypoglycemia and the severity of neurologic dysfunction secondary to hypoglycemia.

Clinical signs that would be expected to result from excessive stimulation of the sympathetic nervous system, such as tremors, panting, anxiety, salivation and muscle twitching, were described by <50% of the cat owners. Most cats were presented only after their owners recognized signs of more severe neurologic dysfunction; ie, mental dullness, weakness, lethargy, stupor or coma. The clinical signs associated with sympathetic nervous system stimulation may not have been seen or recognized by some owners or possibly not demonstrated by cats in this study. Owners may not have been present in the home or cats may have secluded themselves when they felt these signs coming on. Owners are typically warned of subtle signs of hypoglycemia at the time of diagnosis of diabetes mellitus and might also have not presented their cats if these signs resolved on their own or after their cat was fed. Therefore, only cats with clinical signs associated with severe hypoglycemia might be presented for treatment. Blood glucose values identified in the study cats were <49 mg/dl (2.7 mmol/l) when neuronal dysfunction would be expected to occur.⁴⁰

Blood glucose values <20 mg/dl (1.1 mmol/l) (recorded as ‘low’) were more common in cats presenting for stupor or coma (67%) than cats presenting with less severe neurologic signs (29%). Hypoglycemic cats demonstrating the most severe clinical signs on presentation, ie, stupor or coma, were least likely to recover. The predictive value for the blood glucose level on presentation for recovery in cats is unknown; however, 11/14 cats with ‘low’ blood glucose readings did recover from their episode. Those cats that were neurologically improved within 12 h of starting treatment, including those presenting in stupor or coma with glucose <20 mg/dl (1.1 mmol/l), survived to discharge. This finding is similar to that reported in people. In a report evaluating case outcomes in human beings presenting for hypoglycemia, the blood glucose level on admission and duration of hypoglycemia prior to presentation were not correlated with clinical outcome.³⁷ However, the mortality rate was 46% in those individuals presenting in coma/stupor having blood glucose levels <50 mg/dl (2.7 mmol/l) on admission and who remained in a coma/stupor for >24 h, despite normalization of their blood glucose levels.⁴¹ Those cats who survived the hypoglycemic episodes appeared to have completely recovered. Studies in people indicate that those patients recovering from all but the most severe hypoglycemic events do not demonstrate significant changes in their long-term neurologic and cognitive status upon recovery.^41,42 In a study of normal cats in which severe and prolonged hypoglycemia (<1.5 mmol/l for up to 6.6 h) was experimentally induced, brain injury was not identified.⁴³

Excessively high blood glucose measurements (>300 mg/dl) subsequent to IV dextrose treatment in these cats could have affected their recovery. Brain injury after exposure to marked hypoglycemia may be influenced by the level of glycemia achieved during the restoration of blood glucose levels. A study in rats demonstrated that neuronal superoxide production, which is believed to contribute to neuronal damage in hypoglycemic patients, was influenced by the blood glucose concentration achieved in the immediate post-hypoglycemic period.⁴⁴ Similarly, cats experimentally exposed to hypoglycemia and respiratory depression and then treated to hyperglycemic blood levels compared with euglycemia showed substantially greater brain injury than cats in which euglycemia was maintained post-treatment.⁴³ Post-treatment hyperglycemia could have contributed to a slowed or absent recovery in some of these cats. In this same study, the combined exposure of normal cats to hypoglycemia and respiratory depression (elevated PaCO₂ and decreased PaO₂ values) caused brain damage in 10/10 cats vs 2/10 cats that were exposed to the same degree of respiratory depression but remained euglycemic. These findings suggest that the presence of respiratory depression concurrent to hypoglycemia could contribute to more severe brain injury. Cats in stupor or coma could be expected to be demonstrating some degree of respiratory depression, worsening their prognosis for recovery compared with cats that remained more responsive. PaCO₂ and PaO₂ levels were not evaluated in any of the cats in this study to determine if they were demonstrating respiratory depression on presentation.

A number of limitations were present in this study. The sample size of diabetic cats presenting with hypoglycemia was small and the clinical findings and outcomes may not be representative of a larger population of hypoglycemic diabetic cats. In addition, the clinical signs for which cats presented in this study were suspected to be secondary to hypoglycemia. However, a comprehensive diagnostic evaluation was not performed in those cats that did not improve with dextrose therapy to determine if other conditions might be responsible for their ongoing neurologic signs. Patient histories, signs and physical examination findings in these cats, however, were considered to be consistent with a hypoglycemic episode being the cause, although owners may have provided misinformation concerning their pet’s history.

Another limitation to the study was the failure of clinicians to use a standardized neurologic assessment form which could have led to misclassification of their patients’ neurologic status. However, we felt neurologic descriptions were adequately detailed to allow the classification of cats as having stupor or coma compared with demonstrating weakness, lethargy and/or ataxia. Similarly, a standard treatment protocol was not followed, potentially affecting patient outcomes. Finally, one cannot underestimate the role that finances and perceived prognosis had on decisions made by owners to have their patient euthanized. That being said, 6/7 cats that failed to demonstrate neurologic improvement within 12 h of presentation were ultimately euthanized, suggesting that the absence of improvement within 12 h of initiating treatment for hypoglycemia in diabetic cats warrants a poorer prognosis.

Conclusions

Most of the insulin types recommended to treat feline diabetes mellitus were represented in cats presenting for clinical hypoglycemia. Numerous factors, including concurrent illnesses, may have contributed to the development of hypoglycemia in these cats. Cats that demonstrated clinical improvement within 12 h of treatment were more likely to recover, despite their mental status and glucose level on presentation.

Footnotes

Accepted: 26 June 2017

Conflict of interest

The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding

The authors received no financial support for the research, authorship, and/or publication of this article.

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Hypoglycemic episodes in cats with diabetes mellitus: 30 cases (2013–2015)

Abstract

Objectives

Methods

Results

Conclusions and relevance

Introduction

Material and methods

Criteria for case selection

Results

Signalment

Insulin therapy on presentation

History

Signs on presentation

Diagnostic findings

Treatment and outcomes

Discussion

Conclusions

Footnotes

Conflict of interest

Funding

References