Diabetic Ketoacidosis: Pathophysiology, Management and Complications

1992 ◽  
Vol 7 (4) ◽  
pp. 199-211 ◽  
Author(s):  
Susan L. Bratton ◽  
Elliot J. Krane

Diabetic ketoacidosis (DKA) is a common and potentially life-threatening complication of diabetes mellitus, the second most common chronic childhood disease [1]. Prior to the introduction of insulin to clinical medicine by Banting and Best in 1922, DKA had a mortality rate greater than 60% [2]. As insulin was introduced into clinical practice, there was a gradual decrease in mortality associated with DKA over the subsequent 30 years. Recent epidemiological data reveal current mortality varies from 0 to 19% [3,4]. DKA continues to be the most common cause of death in patients younger than 24 years of age; it accounts for as many as 50% of deaths of young diabetic patients [5–7]. In elderly diabetics who have coexisting diseases, DKA carries a high mortality [8]. Despite many advances in the care of diabetic patients, the prevalence of DKA is not declining; it accounts for 14% of all diabetes-related hospital admissions [3, 4, 9]. The incidence of insulin-dependent diabetes mellitus continues to increase worldwide and has roughly doubled in each recent decade [10–13]. Because insulin-dependent diabetes mellitus is increasing, and preventative measures to avoid DKA in diabetic patients have not been successful, the incidence of DKA can also be expected to increase in coming years. Prevention of DKA is the ultimate goal (80% of hospital admissions for DKA occur in treated diabetics) [3,8]. It is necessary for clinicians to understand the pathophysiology and treatment of DKA to care for this increasing diabetic population. We discuss the pathophysiology of diabetic ketoacidosis, its management, and its complications.

1990 ◽  
Vol 123 (5) ◽  
pp. 550-556 ◽  
Author(s):  
Steven Goldstein ◽  
Anna Simpson ◽  
Paul Saenger

Abstract. In addition to increased glycosylation of hemoglobin, abnormalities of other heme proteins such as cytochrome P-450 might also occur in patients with insulin-dependent diabetes mellitus. Antipyrine is a useful marker drug for cytochrome P-450 dependent hepatic drug metabolism. Antipyrine kinetics and urinary excretion of antipyrine metabolites were measured in 14 patients with insulin-dependent diabetes mellitus in poor metabolic control. Improvement in diabetic control in 9 patients, as measured by more normal HbA1 values, led to normalization of plasma antipyrine half-time (t½) and metabolism: the mean antipyrine t½ slowed from 4.7±0.2 (sem) initially to 7.8±0.3 h in these 9 patients and was thus nearly identical to that of normal subjects 8.6±1.0. Antipyrine plasma clearance improved in the 9 diabetic patients whose diabetic control improved. The apparent volume of distribution was normal on both occasions in the diabetic patients. These findings provide a new argument for tight metabolic control in patients with insulin-dependent diabetes mellitus.


2003 ◽  
Vol 17 (2-3) ◽  
pp. 627-633 ◽  
Author(s):  
Handan Boyar ◽  
Belma Turan ◽  
Feride Severcan

Diabetes mellitus (DM) can be accepted as a heterogenous multi organ disorder that can affect various systems of the human body. Disorders include retinopathy, neuropathy, cardiomyopathy, musculoskeletal abnormalities such as diminished bone formation and bone healing retardation. Low bone mineral density is often mentioned as a complication for patients with insulin dependent diabetes mellitus (type I DM). Streptozotocin (STZ) induced diabetic rats are good models for investigation of the complications of insulin dependent diabetes. In the present study, the effects of STZ induced diabetes on the mineral environment of rat bones namely femur and tibia were studied by Fourier transform infrared (FTIR) spectroscopic technique. The results revealed that mineral crystal sizes increased and carbonate content decreased for diabetic femur and tibia. These changes can be due to the formation of osteoporosis which is widely seen in diabetic patients.


1990 ◽  
Vol 11 (10) ◽  
pp. 297-304 ◽  
Author(s):  
H. Peter Chase ◽  
Satish K. Garg ◽  
David H. Jelley

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


2019 ◽  
Vol 7 ◽  
pp. 2050313X1984779 ◽  
Author(s):  
Amjad Halloum ◽  
Shaikha Al Neyadi

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.


2000 ◽  
Vol 2 (6) ◽  
pp. 1-28 ◽  
Author(s):  
Derek W.R. Gray ◽  
Nicolas Titus ◽  
Lionel Badet

The long-term complications of insulin-dependent diabetes mellitus have become a major health care problem, and it is now clear that they arise from inadequate homeostatic control of blood glucose by injected replacement insulin. Transplantation of pancreatic islets is arguably the most logical approach to restoring metabolic homeostasis in people with diabetes. This review looks at the current status of human islet transplantation and the problems that remain. These include: (1) the limited supply of human islet tissue available for transplantation; (2) the adverse effects of current immunosuppressive protocols on diabetic patients; (3) the problems of primary nonfunction of the transplanted islets; (4) the rejection of islets; and (5) the recurrence of autoimmune diabetic disease. Some of the approaches that might solve these problems are then examined: (1) immune modulation to reduce or prevent immune attack by the recipient's immune system; (2) immunoisolation to prevent recognition of the islet graft; (3) induction of tolerance; (4) xenotransplantation using islets derived from animals; and (5) gene therapy.


1995 ◽  
Vol 76 (2) ◽  
pp. 515-521 ◽  
Author(s):  
Gabriele Duran ◽  
Peter Herschbach ◽  
Sabine Waadt ◽  
Friedrich Strian ◽  
Angela Zettler

The reliability, construct validity, and discriminant validity of a new self-report questionnaire, the Questionnaire on Stress in Diabetic Patients, were assessed in a sample of 617 patients with insulin-dependent diabetes mellitus and non-insulin-dependent diabetes mellitus. The 90-item inventory is designed to assess psychosocial stress associated with problems in daily living with diabetes. One of the intended uses is to identify psychosocial factors hampering patient compliance with the necessary treatment regimen. Values of Cronbach alpha ranged from 0.63 to 0.88. The results provide initial evidence for the reliability and validity of the instrument.


2021 ◽  
pp. 107815522110605
Author(s):  
Nasrin Saleh Jouneghani ◽  
John Phillip ◽  
Constantin A Dasanu

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.


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