Severe metabolic acidosis as a consequence of acute starvation in pregnancy

Ketoacidosis is most often due to uncontrolled diabetes mellitus. Similar metabolic changes can occur with poor dietary intake of carbohydrates or prolonged fasting. Metabolic acidosis due to prolonged fasting is rarely described in the literature. We report a case of severe metabolic acidosis as a result of prolonged fasting in pregnancy.     

The Heart in Diabetic Ketoacidosis: A Narrative Review Focusing on the Acute Cardiac Effects and Electrocardiographic Abnormalities

Diabetic ketoacidosis (DKA) is a serious complication of diabetes mellitus. Hyperglycemia, acidosis, and electrolyte imbalances can directly affect the heart by inducing toxicity, impairing myocardial blood flow, autonomic dysfunction, and altering activation and conduction of electrical impulses throughout the heart, increasing the risk of arrhythmias and ischemia. The electrocardiogram is useful in monitoring patients during and after an episode of DKA, as it allows the detection of arrhythmias and guides metabolic correction. Unfortunately, reports on electrocardiographic abnormalities in patients with DKA are lacking. We found two electrocardiographic patterns that are frequently reported in the literature: a pseudo-myocardial infarction and a Brugada Phenocopy. Both are associated with DKA metabolic anomalies and they resolve after treatment. Because of their clinical relevance and the challenge they represent for clinicians, we analyzed the clinical characteristics of these patients and the mechanisms involved in these electrocardiographic findings.     

Ketoacidosis and lactic acidosis – frequent causes of death in chronic alcoholics?

In clinical medicine, severe keto- or lactic adicosis associated with vomiting, nausea, abdominal pain, tachycardia or pathological respiration, has been described in chronic alcoholics. This study reports on fatalities of chronic alcoholics where the cause of death could not be determined by thorough autopsy, histology and toxicology including determination of alcohol concentration. In a first series, acetone was determined in the blood of such chronic alcoholics (n = 24), diabetics with metabolic decompensation (n = 7), cases of hypothermia (n = 7) and controls (n = 218). Among the 24 chronic alcoholics where the cause of death was unknown, 9 cases showed very high levels of acetone (74–400 mg/l). These comprised 6 cases without additional findings and 3 cases where a second patho-mechanism such as intoxication possibly contributed to the cause of death. In a second series, the sum values according to Traub (lactate/glucose) were determined in cerebrospinal liquor of chronic alcoholics with undetermined cause of death (n = 45), diabetics (n = 6) and controls (n = 39). Among the 45 alcoholics, 17 cases showed very high sum values (294–594 mg/dl) including 8 cases where non-lethal intoxications may have contributed to the final outcome. Other causes of a ketoacidosis or lactic acidosis (e.g. diabetes) were excluded in both groups of alcoholics. Consequently, ketoacidosis and lactic acidosis can be the cause of death of chronic alcoholics in a considerable number of cases where no pathomorphological or toxicological changes are present. A scheme for medical and laboratory examination is described. Received: 6 December 1996 / Received in revised form: 30 October 1997     

Post-transplant diabetic ketoacidosis – A possible consequence of immunosuppression with calcineurin inhibiting agents: A case series

Post-transplant diabetes mellitus, a complication due to corticosteroids and the calcineurin inhibitors, cyclosporine and tacrolimus (FK506), is commonly regarded as a form of type-2 (adult-onset) diabetes mellitus. Diabetic ketoacidosis, which requires relative insulin deficiency to impair fatty acid metabolism, is a complication of type-1 diabetes mellitus. We report three patients who presented with diabetic ketoacidosis post-transplant. All three patients presented with severe hyperglycemia, significant ketosis and metabolic acidosis of variable severity. One patient was a renal transplant recipient on a cyclosporine-based regimen. The other two patients were liver transplant recipients receiving either cyclosporine or tacrolimus-based immunosuppression. Both of the liver transplant recipients were found to have moderate to high serum levels of calcineurin inhibitors on presentation. The liver recipient on cyclosporine (Neoral) had a 4 hour post-dose level of 388 ng/ml and the patient on tacrolimus was found to have a trough level of 21.2 ng/ml. Our experience suggests that post-transplant diabetes mellitus, in association with calcineurin inhibition, may result in ketoacidosis either secondary to relative beta cell dysfunction, peripheral insulin resistance, or a combination of the two effects. Post-transplant diabetes mellitus can be an atypical form of adult-onset diabetes with features of both type I and type II diabetes mellitus. Received: 1 February 1999/Revised: 30 September 1999/Accepted: 19 October 1999     

两种胰岛素给药方法治疗糖尿病酮症酸中毒及高渗性昏迷的有效性

目的探讨胰岛素分次皮下注射和胰岛素泵持续皮下注射两种给药方式治疗糖尿病酮症酸中毒及高渗性昏迷患者的有效性研究。方法选取我院自2015年5月~2016年5月间收治的糖尿病酮症酸中毒及高渗性昏迷患者70例作为研究对象,按照随机数字法将其分成两组,即对照组35例患者采用胰岛素分次皮下注射治疗,观察组35例患者采用胰岛素泵持续注射方式,对比两组患者治疗总有效率、空腹血糖(FPG)、餐后2 h血糖水平(2hPBG)、血糖水平达标时间等差异。结果观察组患者治疗总有效率为91.43%,对照组患者仅为71.43%(χ~2=4.629,P0.05);治疗前两组患者FPG、2hPBG水平差异无统计学意义(P0.05),治疗后观察组患者2项指标水平均显著低于对照组,组间数据对比差异有统计学意义(P0.05);观察组患者治疗期间血糖达标时间为(4.25±1.38)d,而对照组为(7.08±2.40)d(t=6.048,P0.05);观察组不良事件发生率为5.71%,对照组为40.00%(χ~2=11.667,P0.05)。结论糖尿病酮症酸中毒及高渗性昏迷患者采用胰岛素泵持续皮下注射给药能够快速恢复机体血糖水平、安全性高,可提升治疗的有效性,因此值得推广使用。     

A case of pegylated interferon alpha-related diabetic ketoacidosis: can this complication be avoided?

We report the case of a 42-year-old woman with chronic hepatitis C (genotype 1), who in June 2004 started therapy with pegylated interferon alpha (PEG-IFNα) plus ribavirin. Two months later, she discontinued treatment because of polydipsia, polyuria and vomiting leading to a marked dehydration. Biochemical data showed type 1 diabetes mellitus with ketoacidosis, and insulin therapy was started. The patient, who before starting PEG-IFN α plus ribavirin therapy tested negative for glutamic acid decarboxylase antibodies (GADAb) and islet cell (ICAb) antibodies, became strongly positive for both autoimmune markers. This case confirms that patients with chronic hepatitis C who do not have baseline markers of pancreatic autoimmunity may develop severe ketoacidosis during treatment with PEG-IFNα, as well as with standard IFNα. In order to avoid this complication, as no guidelines are available and the pancreatic autoimmunity markers are not routinely analysed, we suggest frequent monitoring (e.g., every one to two weeks) of glycaemic values: e.g., every one to two weeks during the first 3 months (when this complication occurs most frequently) and monthly thereafter so as to identify diabetes at an early stage and before the onset of the appearance of severe ketoacidosis, which is life-threatening.     

妇科糖尿病患者围手术期护理

目的:探讨妇科糖尿病患者如何安全渡过围手术期的有效措施。方法:回顾性分析观察组(52例糖尿病患者)与对照组(同期38例非糖尿病患者)术后近期并发症的发生率。结果:1.在术后切口愈合不良、术后发热(>38.5℃)、阴道残端出血方面,两组差异无显著性意义。2.52例糖尿病患者无1例发生酮症酸中毒。结论:糖尿病患者手术要避免发生各种并发症,关键在手术前、术后控制血糖,积极应用抗生素。     

Management of diabetic ketoacidosis in PICU

Objective This study was undertaken to analyze the outcome of children with DKA treated with a modified protocol at a tertiary level teaching hospital PICU in Pune, Maharashtra. Methods We retrospectively analyzed case records of 12 patients (8 males and 4 females) with DKA (11 new and 1 readmission) admitted in our PICU from January 2005 to June 2006. Patients were managed according to a modified protocol (that is with less intensive biochemical monitoring when compared with standard book protocols). Laboratory parameters measured were blood glucose, urinary ketones, electrolytes, urea creatinine, arterial blood gas (ABG) and infectious screen. Treatment included fluid therapy and insulin infusion-0.1 u/Kg short acting intravenously followed by 0.1 u/Kg/hr. No bicarbonate was administered as a bolus. Results Total fluid deficit was corrected slowly over a period of 36 hr. The median time to normalize ABG was 19 hr (5.3-39) while the median time for the urinary ketones to disappear was 1 day (1–3). The child to nurse ratio was 1:2, there were 2 pediatric residents in house all 24 hr with an intensivist and pediatric endocrinologist on call. Conclusion We have shown that when DKA is managed in a PICU setting using modified protocol, the outcome is good and complications such as brain edema can be prevented.     

The Clinical Measures Associated with C-peptide Decline in Patients with Type 1 Diabetes over 15 Years

This study was done to characterize the natural course of C-peptide levels in patients with type 1 diabetes and identify distinguishing characters among patients with lower rates of C-peptide decline. A sample of 95 children with type 1 diabetes was analyzed to retrospectively track serum levels of C-peptide, HbA1c, weight, BMI, and diabetic complications for the 15 yr after diagnosis. The clinical characteristics were compared between the patients with low and high C-peptide levels, respectively. The average C-peptide level among all patients was significantly reduced five years after diagnosis (P < 0.001). The incidence of diabetic ketoacidosis was significantly lower among the patients with high levels of C-peptide (P = 0.038). The body weight and BMI standard deviation scores (SDS) 15 yr after diagnosis were significantly higher among the patients with low C-peptide levels (weight SDS, P = 0.012; BMI SDS, P = 0.044). In conclusion, C-peptide level was significantly decreased after 5 yr from diagnosis. Type 1 diabetes patients whose beta-cell functions were preserved might have low incidence of diabetic ketoacidosis. The declines of C-peptide level after diagnosis in type 1 diabetes may be associated with changes of body weight and BMI.