Cerebral Edema and Ophthalmoplegia Reversed by Mannitol in a New Case of Insulin-Dependent Diabetes Mellitus

PEDIATRICS ◽  
1982 ◽  
Vol 69 (1) ◽  
pp. 87-90
Author(s):  
Bonita Franklin ◽  
John Liu ◽  
Fredda Ginsberg-Fellner
Keyword(s):  
Diabetic Ketoacidosis ◽  
Cerebral Edema ◽  
Insulin Infusion ◽  
Low Dose ◽  
Insulin Dependent Diabetes Mellitus ◽  
Dependent Diabetes Mellitus ◽  
Fluid Restriction ◽  
Insulin Dependent ◽  
Insulin Dependent Diabetic ◽  
Continuous Insulin Infusion

Cerebral edema is a sometimes fatal complication of diabetic ketoacidosis which occurs unpredictably and when biochemical parameters show improvement. A case of a young, newly diagnosed insulin-dependent diabetic boy who developed this complication while receiving a low-dose continuous insulin infusion is reported. Two hours after treatment signs of headache, ophthalmoplegia, and blurred disc margins suggested early cerebral edema. Despite fluid restriction, avoidance of alkali, and phosphate supplementation, cerebral edema ensued three hours later. This complication was then reversed by administration of mannitol. Our patient's ophthalmoplegia, unlike typical diabetic ophthalmoplegia, improved immediately and completely resolved within two weeks after this episode. It is concluded that the use of mannitol in the cerebral edema of diabetic ketoacidosis is beneficial if it is instituted promptly.

scholarly journals Serum IL-1β, IL-2, and IL-6 in Insulin-Dependent Diabetic Children

2006 ◽  
Vol 2006 ◽  
pp. 1-6 ◽  
Author(s):  
Yasar Dogan ◽  
Saadet Akarsu ◽  
Bilal Ustundag ◽  
Erdal Yilmaz ◽  
Metin Kaya Gurgoze
Keyword(s):  
Diabetic Ketoacidosis ◽  
Elevated Serum ◽  
Insulin Dependent Diabetes Mellitus ◽  
Dependent Diabetes Mellitus ◽  
Newly Diagnosed ◽  
Pancreatic Islets Of Langerhans ◽  
Significant Difference ◽  
Long Time ◽  
Insulin Dependent ◽  
Insulin Dependent Diabetic

Insulin-dependent diabetes mellitus (IDDM) is a chronic disease characterized by T-cell-dependent autoimmune destruction of the insulin-producingβcells in the pancreatic islets of Langerhans, resulting in an absolute lack of insulin. T cells are activated in response to islet-dominant autoantigens, the result being the development of IDDM. Insulin is one of the islet autoantigens responsible for the activation of T-lymphocyte functions, inflammatory cytokine production, and development of IDDM. The aim of this study was to investigate serum concentrations of interleukin (IL)-1β, IL-2, IL-6, and tumor necrosis factor (TNF)-αin children IDDM. The study population consisted of 27 children with IDDM and 25 healthy controls. Children with IDDM were divided into three subgroups: (1) previously diagnosed patients (long standing IDDM) (n:15), (2) newly diagnosed patients with diabetic ketoacidosis (before treatment) (n:12), and (3) newly diagnosed patients with diabetic ketoacidosis (after treatment for two weeks) (n:12). In all stages of diabetes higher levels of IL-1βand TNF-αand lower levels of IL-2 and IL-6 were detected. Our data about elevated serum IL-1β, TNF-αand decreased IL-2, IL-6 levels in newly diagnosed IDDM patients in comparison with longer standing cases supports an activation of systemic inflammatory process during early phases of IDDM which may be indicative of an ongoingβ-cell destruction. Persistence of significant difference between the cases with IDDM monitored for a long time and controls in terms of IL-1β, IL-2, IL-6, and TNF-αsupports continuous activation during the late stages of diabetes.

D-[U-11C]glucose uptake and metabolism in the brain of insulin-dependent diabetic subjects

1990 ◽  
Vol 258 (5) ◽  
pp. E805-E812 ◽  
Author(s):  
M. Gutniak ◽  
G. Blomqvist ◽  
L. Widen ◽  
S. Stone-Elander ◽  
B. Hamberger ◽  
...  
Keyword(s):  
Insulin Infusion ◽  
Compartment Model ◽  
Insulin Dependent Diabetes Mellitus ◽  
Dependent Diabetes Mellitus ◽  
Influx Rate ◽  
Positron Emission ◽  
Insulin Dependent ◽  
Arterial Plasma ◽  
Insulin Dependent Diabetic ◽  
The Brain

We used D-[U-11C]glucose to evaluate transport and metabolism of glucose in the brain in eight nondiabetic and six insulin-dependent diabetes mellitus (IDDM) subjects. IDDM subjects were treated by continuous subcutaneous insulin infusion. Blood glucose was regulated by a Biostator-controlled glucose infusion during a constant insulin infusion. D-[U-11C]-glucose was injected for positron emission tomography studies during normoglycemia as well as during moderate hypoglycemia [arterial plasma glucose 2.74 +/- 0.14 in nondiabetic and 2.80 +/- 0.26 mmol/l (means +/- SE) in IDDM subjects]. Levels of free insulin were constant and similar in both groups. The tracer data were analyzed using a three-compartment model with a fixed correction for 11CO2 egression. During normoglycemia the influx rate constant (k1) and blood-brain glucose flux did not differ between the two groups. During hypoglycemia k1 increased significantly and similarly in both groups (from 0.061 +/- 0.007 to 0.090 +/- 0.006 in nondiabetic and from 0.061 +/- 0.006 to 0.093 +/- 0.013 ml.g-1.min-1 in IDDM subjects). During normoglycemia the tracer-calculated metabolism of glucose was higher in the whole brain in the nondiabetic than in the diabetic subjects (22.0 +/- 1.9 vs. 15.6 +/- 1.1 mumol.100 g-1.min-1, P less than 0.01). During hypoglycemia tracer-calculated metabolism was decreased by 40% in nondiabetic subjects and by 28% in diabetic subjects. The results indicate that uptake of glucose is normal, but some aspect of glucose metabolism is abnormal in a group of well-controlled IDDM subjects.

The effect of hyperglucagonaemia on blood glucose concentrations and on insulin requirements during fasting in insulin dependent diabetes mellitus

1983 ◽  
Vol 102 (4) ◽  
pp. 557-560
Author(s):  
W. L. Clarke ◽  
T. W. Melton ◽  
G. M. Bright
Keyword(s):  
Blood Glucose ◽  
Insulin Infusion ◽  
Glucose Production ◽  
Insulin Dependent Diabetes Mellitus ◽  
Dependent Diabetes Mellitus ◽  
Insulin Requirements ◽  
Insulin Dependent ◽  
Insulin Dependent Diabetic ◽  
Blood Glucose Concentrations ◽  
Infusion System

Abstract. The effect of sustained hyperglucagonaemia on blood glucose concentrations and on insulin requirements was evaluated in 6 fasting insulin dependent diabetic subjects whose blood glucose concentrations were being controlled with a closed loop insulin infusion system. Subjects were iv infused initially with either saline or glucagon and subsequently with the other infusate. All determinations were performed following the period during which transient increases in glucagon stimulated glucose production have been reported to occur. Plasma glucagon concentrations were significantly higher during the glucagon study period (491±65 vs 70±13 pg/ml ± sd, P<0.001) as were blood glucose concentrations(104 ± 2 vs 84 ± 7 mg/ml ± sd, P<0.001) and insulin requirements (3.5 to 36.5 vs 0 to 2.3 mU/kg/h, P<0.05). Sustained hyperglucagonaemia continues to have an effect on glucose homeostasis for at least 2 h following the initiation of a continuous infusion.

Methamphetamine use and the risk of diabetic ketoacidosis

2021 ◽  
pp. 002580242110209
Author(s):  
Daniel Lewis ◽  
Corinna van den Heuvel ◽  
Michaela Kenneally ◽  
Roger W Byard
Keyword(s):  
Diabetic Ketoacidosis ◽  
South Australia ◽  
Insulin Dependent Diabetes Mellitus ◽  
Potential Effect ◽  
Insulin Dependent Diabetes ◽  
Dependent Diabetes Mellitus ◽  
Legal Cases ◽  
Insulin Dependent ◽  
Insulin Dependent Diabetic

Diabetic ketoacidosis (DKA) is a life-threatening condition arising in individuals with insulin-dependent diabetes mellitus, associated with hyperglycaemia and hyperketonaemia. While drugs such as methadone, cocaine and certain prescription medications may precipitate DKA, the potential effect of methamphetamine is unclear. Analysis of autopsy and toxicology case files at Forensic Science SA, Adelaide, South Australia, was therefore undertaken from 1 January to 31 December 2019 of all cases where methamphetamine was detected in post-mortem blood samples. There were 94 cases with 11 diabetics ( n = 6 type 1 and n = 5 type 2). Four of the six decedents with type 1 diabetes had lethal DKA (66.7%; age range 30–54 years; average age 44.6 ± 10.5 years; M:F ratio 1:1). This incidence of DKA was higher than that of the general insulin-dependent diabetic population (6%) and also significantly higher than in medico-legal cases (13%; p < 0.05). The clinical and autopsy assessment of insulin-dependent diabetics presenting with DKA should therefore include specific screening for methamphetamine. The increase in both insulin-dependent diabetes and methamphetamine abuse in the community may lead to increases in such cases in medico-legal and health contexts.

Platelet function during continuous insulin infusion treatment in insulin-dependent diabetic patients

Diabetes ◽  
1985 ◽  
Vol 34 (11) ◽  
pp. 1127-1133 ◽  
Author(s):  
R. K. Mayfield ◽  
P. V. Halushka ◽  
H. J. Wohltmann ◽  
M. Lopes-Virella ◽  
J. K. Chambers ◽  
...  
Keyword(s):  
Platelet Function ◽  
Insulin Infusion ◽  
Diabetic Patients ◽  
Insulin Dependent ◽  
Insulin Dependent Diabetic ◽  
Continuous Insulin Infusion

scholarly journals Effector Mechanisms in Low-Dose Streptozotocin-induced Diabetes

1998 ◽  
Vol 6 (1-2) ◽  
pp. 119-128 ◽  
Author(s):  
Miodrag L. Lukic ◽  
Stanislava Stošic-Grujicic ◽  
Allen Shahin
Keyword(s):  
Low Dose ◽  
Insulin Dependent Diabetes Mellitus ◽  
Dependent Diabetes Mellitus ◽  
No Production ◽  
Immune Mediated ◽  
Insulin Dependent ◽  
Streptozotocin Induced Diabetes ◽  
Rats And Mice ◽  
Th 1 ◽  
Diabetes Induction

The cellular and molecular requirements forβ-cell damages in an immune-mediated toxininduced insulin-dependent diabetes mellitus have been studied in the model of multiple low-dose streptozotocin-induced diabetes in rats and mice. It was found that strain-related susceptibility to diabetes induction correlated with a higher level of IL-2, IFN-γ, and TNF-αproduction, whereas such differences were not observed when IL-1 and NO production by macrophages were analyzed; elimination of immunoregulatory RT6+T cells that increases IFN-γproduction, enhances susceptibility to MLD-STZ-induced diabetes; mercury-induced Th-2 cells downregulated the disease; IFN-γ-mediated macrophage activation to produce proinflammatory cytokines rather than NO is an important event in early diabetogenic effects of invading macrophages; inhibition of IL-1 activity downregulates diabetes induction; and generation of NO inβcells appears to be important for diabetogenic effects. Taken together, data indicate that MLD-STZ diabetes is induced by Th-1 lymphocytes that secrete soluble effector molecules that activate macrophages and promote destruction ofβcells possibly by both nitric oxide and nonnitric oxide-mediated mechanisms.

Effects of puberty and diabetes on metabolism of insulin-sensitive fuels

1994 ◽  
Vol 266 (6) ◽  
pp. E885-E891 ◽  
Author(s):  
S. Caprio ◽  
G. Cline ◽  
S. Boulware ◽  
C. Permanente ◽  
G. I. Shulman ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Lipid Oxidation ◽  
Insulin Infusion ◽  
Plasma Free Fatty Acid ◽  
Insulin Dependent Diabetes Mellitus ◽  
Dependent Diabetes Mellitus ◽  
Healthy Controls ◽  
Oxidation Rates ◽  
Acid Protein ◽  
Insulin Dependent

Insulin's ability to stimulate glucose metabolism is reduced during normal puberty; these changes are exaggerated in adolescents with insulin-dependent diabetes mellitus (IDDM). Because the effects of puberty and IDDM on the other actions of insulin have not been established, we studied leucine kinetics (using [1-13C]leucine) and fat metabolism during euglycemic hyperinsulinemia (20 mU.m2.min-1) for 3 h in eight healthy and nine IDDM (HbA1 14 +/- 2%) adolescents and six healthy young adult controls. IDDM subjects received overnight low-dose insulin infusion to normalize fasting glucose. Basal and steady-state insulin values (approximately 240 pM) during the study were similar in all three groups. Insulin-stimulated glucose metabolism was reduced by 40% in healthy adolescents vs. adults (P < 0.05) and by an additional 40% in poorly controlled IDDM (P < 0.05 vs, normal adolescents). Although basal glucose and lipid oxidation rates (measured by indirect calorimetry) were similar in all three groups, when insulin was infused, glucose oxidation increased and lipid oxidation decreased only in the two nondiabetic groups. Similarly, insulin significantly reduced plasma free fatty acid levels only in the nondiabetics. Basal leucine flux (an index of protein degradation) was similar in healthy controls but was markedly increased in IDDM adolescents. Despite similar increments in plasma insulin during the clamp, leucine flux remained higher in IDDM adolescents than in healthy controls. Basal leucine oxidation rates were also increased in IDDM subjects compared with nondiabetic groups and declined to a lesser extent during insulin infusion. We conclude that insulin resistance of puberty is selective for glucose metabolism, sparing amino acid/protein metabolism.(ABSTRACT TRUNCATED AT 250 WORDS)

Diabetic Ketoacidosis in Children and the Role of Outpatient Management

1990 ◽  
Vol 11 (10) ◽  
pp. 297-304 ◽  
Author(s):  
H. Peter Chase ◽  
Satish K. Garg ◽  
David H. Jelley
Keyword(s):  
Diabetic Ketoacidosis ◽  
Hospital Admissions ◽  
Insulin Dependent Diabetes Mellitus ◽  
The United States ◽  
Absolute Number ◽  
Dependent Diabetes Mellitus ◽  
National Commission ◽  
Diabetic Patients ◽  
Intravenous Insulin ◽  
Insulin Dependent

Diabetic ketoacidosis (DKA) is a common complication among children with diabetes, accounting for 14% to 31% of all diabetes-related hospital admissions.1,2 Extrapolation of data from the National Commission on Diabetes3 suggests that there are approximately 160 000 admissions to private hospitals each year in the United States for DKA. The cost of hospitalizations for DKA is over one billion dollars annually. Sixty-five percent of all patients admitted are less than 19 years of age. The incidence of DKA is believed to be declining. However, because the numbers of subjects with insulin-dependent diabetes mellitus is increasing, the absolute number of hospitalizations for DKA is still increasing. It is the single most common cause of death in diabetic patients under 24 years of age.2 The treatment of DKA has changed in recent years, particularly with the use of low-dose continuous intravenous insulin infusion and with the availability of blood pH levels. Severe DKA has been defined as "a state of ketoacidosis with serum bicarbonate decreased to 10 mmol/L or less," or more recently, as a "pH of 7.1 or less."4 The mortality from DKA has been reported to be in the range of 0.5 to 15.4%.3,5 Previous mortality figures were as high as 38%.2

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