Fluid Management of Children Who Have Diabetic Ketoacidosis

1995 ◽  
Vol 16 (8) ◽  
pp. 304-305
Keyword(s):  
Diabetic Ketoacidosis ◽  
Fluid Management ◽  
Insulin Dependent Diabetes Mellitus ◽  
Dependent Diabetes Mellitus ◽  
Hydroxybutyric Acid ◽  
Acetoacetic Acid ◽  
Intracellular Space ◽  
Life Threatening ◽  
Insulin Dependent ◽  
Additional Water

Diabetic ketoacidosis (DKA) is a potentially life-threatening metabolic state that complicates insulin-dependent diabetes mellitus. In the absence of sufficient insulin, glucose is unable to enter cells, and the concentration in plasma increases. When the renal threshold is exceeded (generally at a concentration of about 180 mg/dL), an osmotic diuresis occurs, leading to dehydration. Additional water is lost through hyperventilation (an attempt to compensate for metabolic acidosis), vomiting, and in some cases, diarrhea. Water is drawn from the intracellular space to the plasma to equilibrate the tonicity of the two compartments, bolstering the circulation but producing further intracellular dehydration. Fat is metabolized for fuel because glucose without adequate insulin is not available to cells; beta-hydroxybutyric acid and acetoacetic acid are produced in the process and contribute to acidosis.

scholarly journals Hyperosmolar Hyperglycaemic State and Diabetic Ketoacidosis in Nivolumab-Induced Insulin-Dependent Diabetes Mellitus

2021 ◽  
Author(s):  
Ahmed Osman Saleh ◽  
Ruba Taha ◽  
Shehab Fareed A. Mohamed ◽  
Mohammed Bashir
Keyword(s):  
Diabetes Mellitus ◽  
Diabetic Ketoacidosis ◽  
Autoimmune Diabetes ◽  
Insulin Dependent Diabetes Mellitus ◽  
Dependent Diabetes Mellitus ◽  
Glucose Levels ◽  
Testicular Lymphoma ◽  
Chemotherapy Protocol ◽  
Life Threatening ◽  
Insulin Dependent

Nivolumab is a monoclonal antibody directed against programmed cell death-1 receptor. It has an increasing application in the treatment of various advanced metastatic cancers. The incidence of autoimmune side effects associated with such agents is expected to increase. New-onset autoimmune diabetes mellitus associated with immune checkpoint inhibitor treatment is rare, occurring in less than 1% of patients. Nivolumab-induced diabetes often presents as diabetic ketoacidosis, which could be life-threatening if not recognized and treated promptly. We present the case of a patient who developed severe diabetic ketoacidosis concomitant with hyperosmolar hyperglycaemic state (HHS) after receiving nivolumab for metastatic testicular lymphoma. Pre-nivolumab blood glucose levels were normal, apart from transient hyperglycaemia related to steroids as part of the chemotherapy protocol. The diagnosis was confirmed with extremely low C-peptide in the clinic.

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

scholarly journals Myocardial dysfunction associated with diabetic ketoacidosis in a 5-year-old girl

2019 ◽  
Vol 7 ◽  
pp. 2050313X1984779 ◽  
Author(s):  
Amjad Halloum ◽  
Shaikha Al Neyadi
Keyword(s):  
Diabetes Mellitus ◽  
Diabetic Ketoacidosis ◽  
Brain Edema ◽  
Myocardial Dysfunction ◽  
Insulin Dependent Diabetes Mellitus ◽  
Inotropic Support ◽  
Insulin Dependent Diabetes ◽  
Dependent Diabetes Mellitus ◽  
Insulin Dependent ◽  
New Onset

In this study, we report a case of a 5-year-old girl with new onset of insulin-dependent diabetes mellitus, who presented with severe diabetic ketoacidosis associated with brain edema and severe myocardial dysfunction, needing intubation and inotropic support. To our knowledge, this is the youngest reported case with severe diabetic ketoacidosis complicated with myocardial dysfunction.

Diabetic ketoacidosis as a hallmark of autoimmune diabetes occurring after two cycles of cemiplimab

2021 ◽  
pp. 107815522110605
Author(s):  
Nasrin Saleh Jouneghani ◽  
John Phillip ◽  
Constantin A Dasanu
Keyword(s):  
Diabetes Mellitus ◽  
Diabetic Ketoacidosis ◽  
Immune Checkpoint ◽  
Immune Checkpoint Inhibitors ◽  
Checkpoint Inhibitors ◽  
Insulin Dependent Diabetes Mellitus ◽  
Cutaneous Squamous Cell Carcinoma ◽  
Insulin Dependent Diabetes ◽  
Dependent Diabetes Mellitus ◽  
Insulin Dependent

Introduction Clinical indications of immune checkpoint inhibitors have expanded to a variety of malignancies. Nearly 50% of patients with advanced cutaneous squamous cell carcinoma, respond to the programmed-death 1 inhibitor cemiplimab. To date, insulin-dependent diabetes mellitus has been documented with the use of several immune checkpoint inhibitors but not cemiplimab. Case report We report herein the first case of a patient with cutaneous squamous cell carcinoma who developed diabetic ketoacidosis and insulin-dependent diabetes mellitus following only two cycles of cemiplimab. A score of 6 on the Naranjo nomogram makes the causality relationship between cemiplimab use and the insulin-dependent diabetes mellitus probable. Management and outcome The patient's developed diabetic ketoacidosis was managed with intravenous fluids and intravenous insulin, with a prompt resolution. Cemiplimab was discontinued, and the patient was discharged on long-acting and short-acting insulin therapy, with a follow-up with endocrinology. Discussion/conclusions The mechanism by which cemiplimab caused insulin-dependent diabetes mellitus is most likely due to lack of endogenous insulin production in the setting of immune-mediated loss of pancreatic beta-cells. Patients may benefit from fasting blood glucose monitoring and early immune checkpoint inhibitor discontinuation where elevated serum glucose is detected.

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.

Procalcitonin and White Blood Cells as an Infection Marker in Children with Diabetic Ketoacidosis

2021 ◽  
Vol 70 (12) ◽  
pp. 260-264
Author(s):  
Nur Rochmah ◽  
Muhammad Faizi ◽  
Yudhi Kurniawan ◽  
Latifatu Choirunisa ◽  
Anang Endaryanto ◽  
...  
Keyword(s):  
Diabetic Ketoacidosis ◽  
Blood Cells ◽  
Characteristic Curve ◽  
White Blood Cells ◽  
Insulin Dependent Diabetes Mellitus ◽  
Cross Sectional Study ◽  
Dependent Diabetes Mellitus ◽  
Cross Sectional ◽  
Insulin Dependent ◽  
Infection Marker

Introduction: Diabetic ketoacidosis (DKA), an acute complication of type 1 (insulin dependent) diabetes mellitus (T1DM), can be precipitated by infection. Procalcitonin (PCT) is an accurate marker of bacteremia, sepsis, and inflammation, however white blood cells (WBC) are still often used by clinicians. We aimed to analyze PCT levels and WBC counts in children with DKA.Methods: A cross-sectional study was conducted in Dr. Soetomo General Hospital, Surabaya, Indonesia, between 2015 and 2019. T1DM and DKA diagnosis was based on the International Society for Pediatric and Adolescent Diabetes. PCT levels and WBC counts were measured in samples from patients with and without DKA, and were compared using the Mann-Whitney test.Results: A total of 41 samples were included, with 15 samples (36.6%) from children with DKA, and 26 (63.4%) from children without DKA. PCT levels and WBC counts were significantly higher in those with DKA (p<0.001). The receiver operating characteristic curve analysis of WBC was lower than PCT (0.849 vs. 0.982). PCT had a higher sensitivity and spesificity as an infection marker than WBC (93.3 vs. 86.7; 92.3 vs. 88.5, respectively).Conclusion: PCT is a better infection marker in children with DKA than WBC  

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.

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