Multiple Hypoglycemic Episodes Research Articles

Hypoglycemia imitating cardiac ischemic symptoms A case report and review of literature

Ischemic heart disease is the most common cause of mortality in all low and high-income countries. Diabetes mellitus is also a major public health challenge increasing rapidly worldwide and is reported as an equivalent to coronary heart disease (CHD) in some studies. Hypoglycemia is a common complication in diabetic patients that can stimulate the sympathetic nervous system in its severe form, eventually leading to the destabilization of atherosclerotic plaques and cardiovascular events. Therefore, preventing hypoglycemia is crucial in diabetic patients, especially those with a previous history of CAD, in order to prevent cardiovascular events. In this study, we report a diabetic patient presented with multiple hypoglycemic episodes and chest pain.

Hypoglycemic episodes predict length of stay in patients with acute burns.

Hypoglycemic episodes are associated with worse hospital outcomes. All adult patients admitted to our burn center from 2015 to 2019 were retrospectively reviewed. Patient demographics and burn characteristics were recorded. The primary outcome was mortality, and secondary outcomes were total length-of-stay and intensive care unit length-of-stay. All patients experiencing at least one hypoglycemic episode were compared to patients who did not experience hypoglycemia. There were 914 patients with acute burns admitted during the study period, 33 of which (4%) experienced hypoglycemic episodes. Of these, 17 patients (52%) experienced a single hypoglycemic episode, while the remainder experienced multiple hypoglycemic episodes. Patients with one or more hypoglycemic events were matched to non-hypoglycemic controls using propensity matching. Patients that experienced hypoglycemia had significantly less TBSA involvement (5% vs. 13%,median, p < 0.0002), higher prevalence of diabetes (48% vs. 18%, p < 0.0001), higher mortality (18% vs. 7%, p = 0.01), longer total length-of-stay (22 vs. 8 days, median, p < 0.0001), and longer ICU length-of-stay (12 vs. 0 days, median, p < 0.0001). A single hypoglycemic episode was associated with prolonged total (IRR = 1.91, p < 0.0001) and ICU length-of-stay (IRR = 3.86, p < 0.0001). Hypoglycemia was not associated with higher mortality in the survival analysis (p = 0.46).

10 Hypoglycemic Episodes Predict Length of Stay in Patients with Acute Burns

Abstract Introduction Hypoglycemic episodes are associated with worse hospital outcomes, and their incidence varies by institution. We sought to define the prevalence of hypoglycemic episodes at our burn center and determine their association with hospital outcomes. Methods We retrospectively reviewed all consecutive adult and pediatric patients admitted to our burn center from 2015 to 2019. Patient demographics and burn characteristics were recorded. The primary outcome was mortality, and secondary outcomes were total length of stay (LOS) and intensive care unit LOS (ICU LOS). All patients experiencing hypoglycemic episodes were compared to patients who did not experience hypoglycemic episodes (controls) using two-tailed t, chi-squared, and multivariate logistic and multiple linear regression analyses. Results A total of 914 patients with acute burns were admitted during the study period. Thirty-three patients (4%) experienced hypoglycemic episodes (&amp;lt; 60 mg/dL). Of these, 17 patients (52%) experienced a single hypoglycemic episode, while the remainder (N=16) experienced multiple hypoglycemic episodes. There were no significant differences in age, sex, or presence of inhalation injury between hypoglycemic patients and controls. Patients that experienced a hypoglycemic episode had significantly greater TBSA involvement (23% vs. 11%, p&amp;lt; 0.00), higher prevalence of diabetes (48% vs. 20%, p&amp;lt; 0.00), higher mortality (18% vs. 7%, p=0.01), longer total LOS (39 vs. 13 days, p&amp;lt; 0.00), and longer ICU LOS (28 vs. 4 days, p&amp;lt; 0.00). A single hypoglycemic episode was associated with prolonging total LOS by 19 days (p&amp;lt; 0.00) and ICU LOS by 18 days (p&amp;lt; 0.00). Hypoglycemic episodes were not associated with higher odds of mortality (OR=0.9, 95% CI 0.3–3.0, p &amp;gt;0.05). There were no differences in outcomes between patients with single or multiple hypoglycemic episodes. Patients with multiple hypoglycemic episodes more frequently had a history of diabetes (81% vs. 18%, p&amp;lt; 0.00), and worse glucose control (HbA1c, 9% vs. 7%, p=0.04) compared to patients with single episodes. Conclusions Hypoglycemic episodes were associated with longer total and ICU LOS in our study but did not portend higher mortality. Applicability of Research to Practice Quality improvement efforts to prevent hypoglycemic episodes should focus efforts on known diabetics with high HbA1c levels.

A case report of type 1 diabetes mellitus and factitious hypoglycemia in a patient with Munchausen Syndrome

Munchausen syndrome is rarely considered as a first diagnosis, especially in a type 1 diabetic patient presenting with hyperinsulinemic hypoglycemia. The diagnosis should be considered when episodes of hypoglycemia are persistent, and tests suggest a possible exogenous source of insulin. We report a case of a 26-year-old man with multiple hypoglycemic episodes and a long known diagnosis of diabetes type 1 who was referred to our institution after multiple in and out patient consultations in other institutions. He arrived with persistent hypoglycemia, even after withdrawal of insulin therapy on medical record, but persistent self-administration and misuse, without health care professional knowledge, of insulin therapy. He was diagnosed with factitious hypoglycemia after psychiatric evaluation. The patient improved with psychotherapy and family support as well as strict vigilance of insulin administration.

Ultrasonographic features of insulinoma in six ferrets.

Insulinoma is a functional, insulin-secreting tumor, arising from the beta islet cells of the pancreas. It is one of the most common neoplasms in ferrets and has been associated with clinical signs of hypoglycemia, such as ptyalism, pawing at the mouth, seizures, lethargy, and coma. The ultrasonographic features of insulinoma in ferrets have not been previously reported. The purpose of this retrospective case series study was to describe the ultrasonographic features of confirmed insulinoma in a group of ferrets. Inclusion criteria were abdominal ultrasound examination and histological confirmed insulinoma by surgical biopsy. Six ferrets met the inclusion criteria, all of which had multiple hypoglycemic episodes. Ultrasonographic images were reviewed and the characteristics of the pancreatic nodules were recorded. Twenty-eight pancreatic nodules were observed in the six ferrets and were primarily hypoechoic (89.3%, 25/28) and homogenous (46.4%, 13/28) with a smooth margin (78.6%, 22/28). The distribution of the pancreatic nodules was 46.4% in the left lobe, 50% in the right lobe, and 3.6% in the body of the pancreas. The sizes of the pancreatic nodules varied from 1.5 × 1.5to 4.1 × 5.6mm. All of the pancreatic nodules removed from surgery were histopathologically confirmed as insulinoma. The findings indicated that insulinoma in ferrets could be detected through ultrasonography, which may facilitate diagnosis and preoperative surgical planning.

Severe and multiple hypoglycemic episodes are associated with increased risk of death in ICU patients.

IntroductionIn a randomized controlled trial comparing tight glucose control with a computerized decision support system and conventional protocols (post hoc analysis), we tested the hypothesis that hypoglycemia is associated with a poor outcome, even when controlling for initial severity.MethodsWe looked for moderate (2.2 to 3.3 mmol/L) and severe (<2.2 mmol/L) hypoglycemia, multiple hypoglycemic events (n ≥3) and the other main components of glycemic control (mean blood glucose level and blood glucose coefficient of variation (CV)). The primary endpoint was 90-day mortality. We used both a multivariable analysis taking into account only variables observed at admission and a multivariable matching process (greedy matching algorithm; caliper width of 10−5 digit with no replacement).ResultsA total of 2,601 patients were analyzed and divided into three groups: no hypoglycemia (n =1,474), moderate hypoglycemia (n =874, 34%) and severe hypoglycemia (n =253, 10%). Patients with moderate or severe hypoglycemia had a poorer prognosis, as shown by a higher mortality rate (36% and 54%, respectively, vs. 28%) and decreased number of treatment-free days. In the multivariable analysis, severe (odds ratio (OR), 1.50; 95% CI, 1.36 to 1.56; P =0.043) and multiple hypoglycemic events (OR, 1.76, 95% CI, 1.31 to 3.37; P <0.001) were significantly associated with mortality, whereas blood glucose CV was not. Using multivariable matching, patients with severe (53% vs. 35%; P <0.001), moderate (33% vs. 27%; P =0.029) and multiple hypoglycemic events (46% vs. 32%, P <0.001) had a higher 90-day mortality.ConclusionIn a large cohort of ICU patients, severe hypoglycemia and multiple hypoglycemic events were associated with increased 90-day mortality.Trial registrationClinicaltrials.gov Identifier: NCT01002482. Registered 26 October 2009.

Recurrent hypoglycemia alters hypothalamic expression of the regulatory proteins FosB and synaptophysin

A limiting factor to the clinical management of diabetes is iatrogenic hypoglycemia. With multiple hypoglycemic episodes, the collective neuroendocrine response that restores euglycemia is impaired. In our animal model of recurrent hypoglycemia (RH), neuroendocrine deficits are accompanied by a decrease in medial hypothalamic activation. Here we tested the hypothesis that the medial hypothalamus may exhibit unique changes in the expression of regulatory proteins in response to RH. We report that expression of the immediate early gene FosB is increased in medial hypothalamic nuclei, anterior hypothalamus, and posterior paraventricular nucleus of the thalamus (THPVN) of the thalamus following RH. We identified the hypothalamic PVN, a key autonomic output site, among the regions expressing FosB. To identify the subtype(s) of neuronal populations that express FosB, we screened candidate neuropeptides of the PVN for coexpression using dual fluorescence immunohistochemistry. Among the neuropeptides analyzed [including oxytocin, vasopressin, thyrotropin-releasing hormone, and corticotropin-releasing factor (CRF)], FosB was only identified in CRF-positive neurons. Inhibitory gamma-aminobutyric acid-positive processes appear to impinge on these FosB-expressing neurons. Finally, we observed a significant decrease in the presynaptic marker synaptophysin within the PVN of RH-treated vs. saline-treated rats, suggesting that rapid alterations of synaptic morphology may occur in association with RH. Collectively, these data suggest that RH stress triggers cellular changes that support synaptic plasticity, in specific neuroanatomical sites, which may contribute to the development of hypoglycemia-associated autonomic failure.

Caution Is Urged in Elderly Diabetes Care

Caution Is Urged in Elderly Diabetes Care

Dissociation of hypothalamic noradrenergic activity and sympathoadrenal responses to recurrent hypoglycemia.

This study evaluated whether attenuation of sympathoadrenal responses to recurrent hypoglycemia is mediated by diminished noradrenergic activity in the hypothalamus. Male Sprague-Dawley rats received either once daily insulin (1.0 units/kg) injections or an equal administration of saline for 3 days. Both groups received an administration of insulin on the fourth day, during which blood glucose and plasma catecholamines were determined, and extracellular norepinephrine (NE) in the ventromedial hypothalamus (VMH) or paraventricular hypothalamic nucleus (PVN) was monitored with microdialysis. The peak response of plasma epinephrine to insulin-induced hypoglycemia (nadir approximately 3.2 mmol/l) was significantly reduced during the fourth hypoglycemic episode (774 +/- 134 pg/ml) compared with the first episode (2,561 +/- 410 pg/ml, P < 0.001). Baseline levels of extracellular NE were elevated approximately 25% (P = 0.07) in the VMH and approximately 46% (P = 0.03) in the PVN after multiple hypoglycemic episodes. There was no difference in noradrenergic activity during the first or fourth hypoglycemic episode in either brain area. The reduced sympathoadrenal output after recurrent hypoglycemia is likely postsynaptic from hypothalamic NE release or is mediated via a collateral pathway.

Effects of Repetitive Hypoglycemia on Neuroendocrine Response and Brain Tyrosine Hydroxylase Activity in the Rat

Hypoglycemia-associated autonomic failure (HAAF) is a syndrome of acute adaptation to a metabolic stressor, in which neuroendocrine responses to repetitive hypoglycemic bouts are blunted. The CNS mechanisms that contribute to HAAF are unknown. In the present study, we modeled HAAF in the rat and measured the activity of tyrosine hydroxylase (TH) as an index of acute noradrenergic activation, to test the hypothesis that noradrenergic activation of the hypothalamus might be impaired. In association with a significant counter-regulatory response to a single bout of hypoglycemia (elevated corticosterone, catecholamines, and glucagon), TH activity was elevated overall in brainstem NE cell body areas and hypothalamus. With multiple hypoglycemic episodes in a 24 h period, the counter-regulatory response was blunted, and hypothalamic TH activity was comparable to that of saline-infused controls. In a similar paradigm, multiple bouts of CNS neuroglucopenia did not blunt the hyperglycemic or corticosterone responses, and were required for elevation of TH activity. This alternate response pattern suggests that insulin-induced hypoglycemia and cerebral neuroglucopenia represent somewhat different metabolic stressors at the CNS.