Hospital Admissions For Diabetic Ketoacidosis Research Articles

Diabetic Ketoacidosis in Prisoners Without Access to Insulin

To assess the cause and clinical severity of diabetic ketoacidosis in male prisoners hospitalized in New York City. Retrospective chart review. A municipal hospital in New York City. Forty-nine adult male prisoners with a total of 54 hospital admissions for diabetic ketoacidosis between January 1, 1989, and June 30, 1991. Charts were reviewed for diabetic and medical history, time from arrest until hospitalization, cause of diabetic ketoacidosis, admission laboratory data, and hospital course. Thirty-eight (70%) of the 54 admissions for diabetic ketoacidosis among prisoners occurred because prisoners had not received insulin during the period immediately following arrest (mean number of days from arrest until hospitalization was 2.5). All of these individuals had a history of insulin-dependent diabetes and were reportedly compliant with their insulin regimen at the time of arrest. Admission laboratory data for this group of prisoners included a mean serum glucose level of 27.4 mmol/L (495 mg/dL) and a mean serum bicarbonate level of 14.4 mmol/L. Mean number of days in the hospital was 3.4 including a mean of 1 day in an intensive care unit. Inadequate access to medication results in serious sequelae for recently arrested prisoners in New York City with insulin-dependent diabetes. Access to health care for recently arrested prisoners needs to be improved.

Diabetic Ketoacidosis: Pathophysiology, Management and Complications

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.

Relationship Between Severity of Hyperglycemia and Metabolic Acidosis in Diabetic Ketoacidosis

We evaluated 114 hospital admissions for diabetic ketoacidosis (occurring in 78 patients) retrospectively by using the Mayo Clinic medical records system. Initial plasma glucose and serum bicarbonate values were examined by using regression analysis. No correlation was found between these two measurements (r = -0.03). The reason for this dissociation between hyperglycemia and hyperketonemia needs further elucidation, but it may be related to impaired hepatic glucose production in some patients.

Subcutaneous peritoneal access device for type I diabetic patients nonresponsive to subcutaneous insulin.

Three type I diabetic patients nonresponsive to subcutaneous insulin were implanted with a subcutaneous peritoneal access device. In these patients, multiple subcutaneous injections had been unable to prevent recurrent hospital admissions for diabetic ketoacidosis. The patients were responsive to intravenous insulin but had limited accessible peripheral veins. Complications of thrombosis and/or septicemia from permanent central venous catheters prevented the long-term use of this route. The peritoneal access device was implanted subcutaneously adjacent to the umbilicus with its insulin delivery catheter terminating in the peritoneal space. Transcutaneous injection of insulin into the subcutaneous access port resulted in the same quantity of insulin entering the peritoneal space. Using a mixture of regular and protamine zinc insulin in a ration of 1:1 resulted in acute increases in plasma free insulin concentration with meals and a declining background level postprandially. All peritoneal access devices have been functioning well for at least 2 mo and in one of the implanted diabetic subjects, it has been in continuous use for 5 mo with no evidence of peritonitis or resistance to peritoneal insulin. These results suggest that a subcutaneous peritoneal access device may provide an alterative insulin delivery route for patients who are nonresponsive to subcutaneous insulin injections.