Severe Ketoacidosis Research Articles

Management of Type 1 Diabetes in the Hospital Setting.

The purpose of this article was to review recent guideline recommendations on glycemic target, glucose monitoring, and therapeutic strategies, while providing practical recommendations for the management of medical and surgical patients with type 1 diabetes (T1D) admitted to critical and non-critical care settings. Studies evaluating safety and efficacy of insulin pump therapy, continuous glucose monitoring, electronic glucose management systems, and closed loop systems for the inpatient management of hyperglycemia are described. Due to the increased prevalence and life expectancy of patients with type 1 diabetes, a growing number of these patients require hospitalization every year. Inpatient diabetes management is complex and is best provided by a multidisciplinary diabetes team. In the absence of such resource, providers and health care staff must become familiar with the features of this condition to avoid complications such as severe hyperglycemia, ketoacidosis, hypoglycemia, or glycemic variability. We reviewed most recent guidelines and relevant literature in the topic to provide practical recommendations for the inpatient management of patients with T1D.

AB076. Heterozygous carriers of succinyl-CoA:3-oxoacid CoA transferase deficiency can develop severe ketoacidosis

Succinyl-CoA:3-oxoacid CoA transferase (SCOT, gene symbol OXCT1) deficiency is an autosomal recessive disorder in ketone body utilization that results in severe recurrent ketoacidotic episodes in infancy, including neonatal periods. More than 30 patients with this disorder have been reported and to our knowledge, their heterozygous parents and siblings have had no apparent ketoacidotic episodes. Over 5 years (2008–2012), we investigated several patients that presented with severe ketoacidosis and identified a heterozygous OXCT1 mutation in four of these cases (Case1 p.R281C, Case2 p.T435N, Case3 p.W213*, Case4 c.493delG). To confirm their heterozygous state, we performed a multiplex ligation-dependent probe amplification analysis on the OXCT1 gene which excluded the presence of large deletions or insertions in another allele. A sequencing analysis of subcloned full-length SCOT cDNA showed that wild-type cDNA clones were present at reasonable rates to mutant cDNA clones. Over the following 2 years (2013–2014), we analyzed OXCT1 mutations in six more patients presenting with severe ketoacidosis (blood pH ≦7.25 and total ketone body ≧10 mmol/L) with non-specific urinary organic acid profiles. Of these, a heterozygous OXCT1 mutation was found in two cases (Case5 p.G391D, Case6 p.R281C). Moreover, transient expression analysis revealed R281C and T435N mutants to be temperature-sensitive. This characteristic may be important because most patients developed ketoacidosis during infections. Our data indicate that heterozygous carriers of OXCT1 mutations can develop severe ketoacidotic episodes in conjunction with ketogenic stresses.

Screening for neonatal diabetes at day 5 of life using dried blood spot glucose measurement

Aims/hypothesisThe majority of infants with neonatal diabetes mellitus present with severe ketoacidosis at a median of 6 weeks. The treatment is very challenging and can result in severe neurological sequelae or death. The genetic defects that cause neonatal diabetes are present from birth. We aimed to assess if neonatal diabetes could be diagnosed earlier by measuring glucose in a dried blood spot collected on day 5 of life.MethodsIn this retrospective case–control study we retrieved blood spot cards from 11 infants with genetically confirmed neonatal diabetes (median age of diagnosis 6 [range 2–112] days). For each case we also obtained one (n = 5) or two (n = 6) control blood spot cards collected on the same day. Glucose was measured on case and control blood spot cards. We established a normal range for random glucose at day 5 of life in 687 non-diabetic neonates.ResultsAll 11 neonates with diabetes had hyperglycaemia present on day 5 of life, with blood glucose levels ranging from 10.2 mmol/l to >30 mmol/l (normal range 3.2–6.0 mmol/l). In six of these neonates the diagnosis of diabetes was made after screening at day 5, with the latest diagnosis made at 16 weeks.Conclusions/interpretationNeonatal diabetes can be detected on day 5 of life, preceding conventional diagnosis in most cases. Earlier diagnosis by systematic screening could lead to prompt genetic diagnosis and targeted treatment, thereby avoiding the most severe sequelae of hyperglycaemia in neonates.

Heterozygous carriers of succinyl-CoA:3-oxoacid CoA transferase deficiency can develop severe ketoacidosis

Succinyl-CoA:3-oxoacid CoA transferase (SCOT, gene symbol OXCT1) deficiency is an autosomal recessive disorder in ketone body utilization that results in severe recurrent ketoacidotic episodes in infancy, including neonatal periods. More than 30 patients with this disorder have been reported and to our knowledge, their heterozygous parents and siblings have had no apparent ketoacidotic episodes. Over 5years (2008-2012), we investigated several patients that presented with severe ketoacidosis and identified a heterozygous OXCT1 mutation in four of these cases (Case1 p.R281C, Case2 p.T435N, Case3 p.W213*, Case4 c.493delG). To confirm their heterozygous state, we performed a multiplex ligation-dependent probe amplification analysis on the OXCT1 gene which excluded the presence of large deletions or insertions in another allele. A sequencing analysis of subcloned full-length SCOT cDNA showed that wild-type cDNA clones were present at reasonable rates to mutant cDNA clones. Over the following 2years (2013-2014), we analyzed OXCT1 mutations in six more patients presenting with severe ketoacidosis (blood pH ≦7.25 and total ketone body ≧10mmol/L) with non-specific urinary organic acid profiles. Of these, a heterozygous OXCT1 mutation was found in two cases (Case5 p.G391D, Case6 p.R281C). Moreover, transient expression analysis revealed R281C and T435N mutants to be temperature-sensitive. This characteristic may be important because most patients developed ketoacidosis during infections. Our data indicate that heterozygous carriers of OXCT1 mutations can develop severe ketoacidotic episodes in conjunction with ketogenic stresses.

Clinical characteristics, beta-cell dysfunction and treatment outcomes in patients with A − β + Ketosis-Prone Diabetes (KPD): The first identified cohort amongst Asian Indians

ObjectiveKetosis-prone diabetes (KPD), an atypical form of diabetes, has emerged as a heterogeneous syndrome in multiple ethnic groups. The objectives of this study were to look into the clinical characteristics of adult Asian Indian patients with recently diagnosed, antibody negative diabetes presenting with unprovoked ketoacidosis (A−β+ KPD) and to determine the natural course of recovery of beta-cell functions on serial follow-up over one year. Research design and methodsNewly diagnosed adult diabetes patients (n=11) with suspected KPD (A−β+) were prospectively studied over a period of 1-year with serial evaluations of clinical, biochemical and beta-cell secretion characteristics. These were compared with a control group (n=23) of KPD (A+β−) (classical Type 1A diabetes) with similar presentation. Beta-cell secretion was assessed by fasting and stimulated C-peptide values after a standard mixed meal challenge. Glycaemic control and treatment outcomes were also documented. ResultsIn comparison to the A+β− KPD controls, the A−β+ KPD patients had a significantly older age, higher BMI, stronger family history of type 2 diabetes, more severe ketoacidosis and higher fasting and stimulated C-peptide level at presentation. On serial follow-up, the patients with KPD achieved complete recovery of their beta-cell function with remission from insulin-dependence within 3–4months without further recurrences of DKA. ConclusionsThis is the first reported series of A−β+ KPD from India. The phenotype of Indian A−β+ KPD patients differs from their Western counterparts in that they are relatively younger and leaner, though the male preponderance and natural history of recovery of beta-cell dysfunction bears similarity.

Hyperglycaemia-related complications at the time of diagnosis can cause permanent neurological disability in children with neonatal diabetes

BackgroundChildren with neonatal diabetes often present with diabetic ketoacidosis and hence are at risk of cerebral oedema and subsequent long‐term neurological deficits. These complications are difficult to identify because neurological features can also occur as a result of the specific genetic aetiology causing neonatal diabetes.Case reportsWe report two cases of neonatal diabetes where ketoacidosis‐related cerebral oedema was the major cause of their permanent neurological disability. Case 1 (male, 18 years, compound heterozygous ABCC8 mutation) and case 2 (female, 29 years, heterozygous KCNJ11 mutation) presented with severe diabetic ketoacidosis at 6 and 16 weeks of age. Both had reduced consciousness, seizures and required intensive care for cerebral oedema. They subsequently developed spastic tetraplegia. Neurological examination in adulthood confirmed spastic tetraplegia and severe disability. Case 1 is wheelchair‐bound and needs assistance for transfers, washing and dressing, whereas case 2 requires institutional care for all activities of daily living. Both cases have first‐degree relatives with the same mutation with diabetes, who did not have ketoacidosis at diagnosis and do not have neurological disability.DiscussionKetoacidosis‐related cerebral oedema at diagnosis in neonatal diabetes can cause long‐term severe neurological disability. This will give additional neurological features to those directly caused by the genetic aetiology of the neonatal diabetes. Our cases highlight the need for increased awareness of neonatal diabetes and earlier and better initial treatment of the severe hyperglycaemia and ketoacidosis often seen at diagnosis of these children.

Efficacy and safety of incretin-based drugs in patients with type 1 diabetes mellitus: A systematic review and meta-analysis.

In patients with type 2 diabetes, incretin-based therapies can improve glucose control without increased weight gain or hypoglycemia. Incretin-based drugs added to insulin therapy in type 1 diabetes (T1DM) have also been tried in many studies. However, the results were controversial. We thus performed a meta-analysis to assess the efficacy and safety of incretin-based therapies in patients with T1DM. We systematically searched Medline, EMBASE, and Cochrane Central Register of Controlled Trials for relevant studies published before August 25, 2016. Data was extracted by two independent reviewers. The main outcomes included glycosylated hemoglobin (HbA1c), insulin dose, weight, hypoglycemia, ketosis and ketoacidosis. All pooled data were assessed using random-effects model. Twelve randomized controlled trials with a total of 2903 individuals were finally included into the meta-analysis. Incretin-based drugs could significantly reduce HbA1c (MD -0.20, 95% CI -0.30 to -0.10), weight (MD -2.83, 95% CI -4.00 to -1.65) and insulin dose (MD -4.55, 95% CI -6.15 to -2.94). Furthermore, incretin-based drugs did not increase relative risk of severe hypoglycemia (RR 0.79, 95% CI 0.58 to 1.06), ketosis (RR 1.37, 95% CI 0.95 to 1.97) and ketoacidosis (RR 2.62, 95% CI 0.31 to 21.99). Incretin-based treatment in patients with T1DM may improve glycemic control and reduce insulin dose and weight without increasing the risk of serious adverse event, such as severe hypoglycemia, ketosis or ketoacidosis. The current evidence for the aforementioned adverse effects, however, is weak. A rigorous monitoring of these adverse events should be implemented in well-designed observational studies.

Severe hypoglycaemic ketoacidosis in a patient with adrenal crisis

Severe hypoglycaemic ketoacidosis in a patient with adrenal crisis

Making health technology assessment more dynamic – Temporal trend analysis to capture performance trajectories

ObjectivesHealth technology assessment (HTA) has an increasing role in evaluating not only drugs, but also medical devices. Assessing medical devices is more challenging as outcomes tend to improve substantially over time. This paper analyzes clinical outcomes over time of insulin pump therapy in adult type 1 diabetes. Meta-regression was used to capture outcome trends while considering innovation theory. MethodsA systematic review of 4.297 studies was conducted covering a 35 year time period. To meet the need for a more dynamic evaluation method, temporal trend analysis was applied based on meta-regression of three extracted outcome parameters: HbA1c, incidence of severe hypoglycemia and ketoacidosis. ResultsThe systematic review included 150 studies. Performance improvement in HbA1c and ketoacidosis was rapid during the 1980 and 90s. Thereafter the improvement trajectory of insulin pumps measured by HbA1c, ketoacidosis or severe hypoglycemia was essentially flat. Meta-regression of several covariates was performed showing publication year to be statistically significant. Retrospective recruitment and the percentage of female patients were also statistically significant. A technology cycle model analysis revealed convergence to a dominant design by the end 1990s, followed by slower progress in outcomes. ConclusionsInsulin pump technology currently does not offer an improving performance trajectory according to key indicators HbA1c, incidence of severe hypoglycemia and ketoacidosis, but compares well to manual insulin injections in terms of quality of life. Applying temporal trend analysis is especially valuable in an early technology cycle stage when uncertainty is high, and when predicted improvements in future performance can influence the choice of technology.

A case of severe bovine ketoacidosis in a lactating female

A case of severe bovine ketoacidosis in a lactating female

Risk factors for cerebral oedema in children and adolescents with diabetic ketoacidosis

ABSTRACTCerebral oedema (CO) is a rare life-threatening complication of diabetic ketoacidosis (DKA) in children. We analysed the biochemical and therapeutic risk factors for CO in DKA by a retrospective review of 256 children hospitalized for DKA between February 2003 and March 2015. The demographic characteristics, biochemical variables and therapeutic interventions were compared between the patients with and without CO. CO was observed in 22 (8.6%) of the 256 subjects included in the study. One of these patients (5%) had a fatal outcome and two patients (9%) survived with neurological consequences. CO was significantly associated with severe DKA: lower initial venous pH (p < 0.001) and bicarbonate (p < 0.001), higher initial blood glucose (p < 0.01), urea level (p < 0.05) and baseline serum osmolality (р < 0.05). During the treatment of DKA, low serum phosphate level was found to be significantly associated with CO (p < 0.05). We also found significant dependence between the development of CO and the initiation of treatment for DKA in another facility before hospitalization in our hospital (p < 0.05), bicarbonate application (p < 0.001), higher fluid volume infused initially (p < 0.01) and delayed potassium substitution (p < 0.01). Severe ketoacidosis, hyperglycaemia and dehydration at presentation, and low serum phosphate during treatment are significantly related to CO formation in children with DKA. The initial severe acidosis and hyperglycaemia probably cause brain injury which progresses into CO in the course of developing hypophosphatemia and cerebral hypervolemia.

Clinical characteristics of type 1 diabetes mellitus in Taiwanese children aged younger than 6 years: A single-center experience.

Cases of type 1 diabetes mellitus in children aged younger than 6 years in Taiwan has increased in the past 10 years. This retrospective study aimed to review the management experience of such patients in a single center. From January 2004 to June 2015, 52 newly diagnosed diabetic children younger than 6 years who had regular follow-up for >1 year were enrolled, as well as 94 older diabetic children for comparison. Their medical records were thoroughly reviewed. The most common symptoms and signs were polyuria, polydipsia, dry lips, weight loss, and nocturia. Among the children younger than 6 years, 87% had ketoacidosis upon diagnosis-significantly higher than that of the older age group-and 88% had at least one islet cellautoantibody detected. Their serum C-peptide levels were significantly lower and the frequency of insulin autoantibodies detected was significantly higher compared with the older age group (37% vs. 10%). The remission rate of the young diabetic patients was significantly lower than that of the older age group (40% vs. 59%), but there was no difference in time of onset and duration of remission between the two groups. Autoimmune destruction of pancreatic β-cells is an important cause of type 1 diabetes mellitus in Taiwanese children aged younger than 6 years. These patients usually have a low insulin reserve and severe ketoacidosis upon diagnosis. A high index of suspicion in the presence of classic symptoms of diabetes in young children is important to prevent complications.

The clinical potential of low-level C-peptide secretion

ABSTRACTIntroduction: In all forms of diabetes, especially so in Type 1 diabetes (T1D), beta cell function is crucial for the course. The interest for residual beta cell function has been meagre, but increased in recent years with interventions to preserve function.Areas covered: Importance and clinical use of C-peptide in Type 1 diabetes. Data for this review were identified by searches of PubMed, and references from relevant articles using the search terms: “type 1 diabetes”, “C-peptide”, “beta cell function”, “HbA1c”, quality of life”, “complications”. s and reports from meetings were not included.Expert commentary: C-peptide may help to get a correct diagnosis, and it is of practical clinical value to know degree of residual insulin secretion to diminish the risk of severe hypoglycaemia and ketoacidosis. Evidence shows that even a quite reduced beta cell function may play an important role for quality of life, for metabolic balance/control, possibility to avoid complications and even for long-term survival. Furthermore, the evidence is increasing for C-peptide being a hormone per se.

It's education, Jim, but not as we know it

It's education, Jim, but not as we know it

Does β-Cell Autoimmunity Play a Role in Cystic Fibrosis–Related Diabetes? Analysis Based on the German/Austrian Diabetes Patienten Verlaufsdokumentation Registry

Research on β-cell autoimmunity in cystic fibrosis (CF)-related diabetes (CFRD) is still rare. We aimed to analyze the frequency of β-cell autoimmunity and the influence on age at diabetes onset, insulin requirement, type of insulin therapy, and hypoglycemic or ketoacidotic events in patients with CFRD compared with antibody-negative patients with CFRD in the Diabetes Patienten Verlaufsdokumentation (DPV) registry. We analyzed data of 837 patients with CFRD in the German/Austrian DPV database by multivariable mixed-regression modeling. In our cohort, 8.5% of patients with CFRD (n = 72) were found to be β-cell antibody positive. There was a female preponderance in this patient group: 65.3 vs. 57.6%. Diabetes onset (median [interquartile range]) was earlier (14.00 [10.15-15.90] vs. 16.10 [13.50-21.20] years; P < 0.005), and insulin dose/kg body weight was higher (0.95 [0.61-1.15] vs. 0.67 [0.33-1.04] IU/kg; P < 0.05). There were also differences in the type of insulin treatment. Insulin pump therapy was used significantly more often in patients with CFRD with β-cell autoimmunity (18.2 vs. 6.4%; P < 0.05). The differences for multiple daily injections (ICT) and conventional therapy (CT) were not significant (ICT: 67.7 vs. 79.0%; CT: 15.2 vs. 14.6). Oral antidiabetic agents were rarely used in both groups. Rate of severe hypoglycemia with coma and rate of ketoacidosis were higher in antibody-positive patients (hypoglycemia with coma: 8.0 vs. 1.4, P < 0.05; ketoacidosis: 9.3 vs. 0.9, P < 0.05). Presence of β-cell autoantibodies in our cohort of patients with CFRD (8.5%) appeared to be greater than in the general population and was associated with female sex, earlier onset of diabetes, and higher insulin requirement. Insulin pump therapy was used significantly more often in patients with β-cell antibodies. Severe hypoglycemia and ketoacidosis were significantly more frequent in CFRD with β-cell autoimmunity compared with β-cell antibody-negative patients with CFRD.

Analysis of clinical phenotype and ACAT1 gene mutation in a family affected with beta-ketothiolase deficiency

To investigate the clinical phenotype and ACAT1 gene mutation in a family affected with beta-ketothiolase deficiency (BKTD). Clinical features and laboratory test data were collected. The probands were monozygotic twin brothers. Genomic DNA was isolated from peripheral blood leukocytes obtained from the probands and their family members. Molecular genetic testing of the ACAT1 gene was carried out. The probands have presented with fever, vomiting and severe ketoacidosis. By arterial blood gas testing, pH was determined to be 7.164, bicarbonate was 4.0 mmol/L, and urine ketone was ++++. Urinary organic acid gas chromatography-mass spectrometry analysis showed excessive excretion of 3-hydroxybutyric acid, 2-methyl-3-hydroxybutyric acid and tiglylglycine. Increased 3-hydroxybutyrylcarnitine (C4-OH), tiglylcarnitine(C5:1) and 3-hydroxyisovalerylcarnitine (C5-OH) levels. The clinical phenotype of proband's parents were both normal, but an elder sister turned out to be an affected patient. Genetic analysis has identified two heterozygous mutations [c.622C>T(p.R208X) and c.653C>T (p.S218F)] in the proband, which were respectively detected in the mother and father. The c.653C>T (p.S218F) mutation was not found among the 100 healthy controls and has not been included in the Human Gene Mutation Database(HGMD). The primary clinical manifestations of BKTD is ketoacidosis. Urine organic acid and blood acylcarnitine analyses play an important role in the diagnosis of the disease. The compound heterozygous of ACAT1 gene mutations probably underlie the BKTD in our patient.

Diabetes Technology and Therapy in the Pediatric Age Group.

We continue to see tremendous advances in both research and clinical translation of diabetes technology and therapeutics in the pediatric age group. This year's selection of manuscripts in the article spans the full range of ages in pediatrics and includes novel glucose monitoring and closed-loop systems as well as translation of medications commonly used in adults into the pediatric population. As new technologies are researched and applied clinically, reports on use of current diabetes technologies including the effectiveness of pumps compared to multiple daily injections, use of continuous glucose monitoring (CGM) in preterm infants and data on intermittently scanned CGM (isCGM) become available. These real-world data (1) are very important for clinicians and researchers to better understand how to most effectively translate new developments to best solve the challenges our patients face on a daily basis. Further data are reported on closed-loop control systems, including predicted low-glucose suspend systems and multiple studies in which closed-loop systems were challenged by exercise, as this is a real-world problem for children and adolescents with diabetes and more data are required to best manage this in an outpatient setting. In addition to diabetes technology, this year's articles remind us of the long-term complications of diabetes and the increased future risk of cardiovascular disease and mortality (2–4). Reports are included on therapies translated from adult to pediatric populations in studies designed to decrease the risk of long-term vascular complications. Finally, because the delay, prevention, and curing of diabetes remain the ultimate goals in diabetes research, the international TrialNet Oral Insulin trial is summarized and raises hypotheses to focus future research in type 1 diabetes (T1D). To select these 13 articles focused on diabetes technology and therapeutics in the pediatric age group, we conducted a Medline search for articles dealing with the following topics: diabetes technology, insulin pump therapy (CSII), continuous glucose monitoring (CGM), closed-loop systems, and new therapies in T1D relating to the pediatric age group (0–18 years). We focused on key articles that offer some insight into these issues and were published between July 1, 2017, and June 30, 2018. Key Articles Reviewed for the Article Association of insulin pump therapy vs insulin injection therapy with severe hypoglycemia, ketoacidosis, and glycemic control among children, adolescents, and young adults with type 1 diabetes Karges B, Schwandt A, Heidtmann B, Kordonouri O, Binder E, Schierloh U, Boettcher C, Kapellen T, Rosenbauer J, Holl RW JAMA 2017;318: 1358–1366

Severe Ketoacidosis in a Patient with an Eating Disorder.

Severe ketoacidosis with a blood pH below 7.0 is only rarely seen in other diseases except type 1 diabetes. This paper reports a case of severe ketoacidosis secondary to an eating disorder. A 46-year-old woman presented to the emergency department with an acute onset of shortness of breath. She has a history of an eating disorder, an anxiety disorder, and hypothyroidism. Her body mass index was 19. Examination of the initial vital signs revealed the following: pulse, 91 beats/min; body temperature, 34.9℃; respiratory rate, 35 breaths/min; oxygen saturation, 100% on room air; and blood pressure, 130/70 mmHg. Urinalysis revealed specific gravity of >1.030, pH of 5.5, negative results for glucose, and positive results for ketone bodies (>150 mg/dL). Her serum glucose level was 4.9 mmol/L. Venous blood gas analysis revealed the following: pH, 6.96; HCO3−, 5 mmol/L, pCO2, 22 mmHg; base deficit, 27 and anion gap, 21. the patient showed a high anion gap metabolic acidosis with proper respiratory compensation. Results of the blood analysis are shown in Table 1. The osmolar gap was 20, which suggested unmeasured anions. However, tests for ethanol, salicylate, ethylene glycol, and methanol levels were negative. The serum ketone test was positive. These laboratory parameters made us rule out diabetic ketoacidosis and alcoholic ketoacidosis as the cause of the metabolic acidosis. Initially, the patient received a 5% dextrose solution in normal saline (D5W NS). After 12 hours of hospitalization on D5W NS, venous blood gas analysis revealed improved results: pH, 7.18; HCO3−, 5 mmol/L; and pCO2, 13 mmHg, with a base deficit of 23. TABLE 1 Biochemical markers Initially, the family and the patient told us that the patient had been doing much better in the last 2 weeks regarding her eating habits. We asked her repeatedly and she finally admitted to giving her food to her dog underneath the table. Moreover, she had been taking stool laxatives. In a patient with ketonemia, low glucose levels excluded diabetic ketoacidosis as the cause of severe metabolic acidosis.1 Negative results for laboratory tests for toxicology and toxic alcohol levels led us to consider starvation as the etiology of the acid-base imbalance.2 Ketoacidosis secondary to starvation is due to diminished insulin secretion that leads to an increase in lipolysis and ketogenesis.3 Eating disorders not otherwise specified are a category of eating disorder that includes patients with early aberrant eating patterns and weight management habits who do not meet the criteria for anorexia or bulimia nervosa.4 It occurs in approximately 3-5% of women aged between 15 and 30 years in Western countries.5 Patients with bulimia ten to abuse laxatives. It prevents the absorption of calories, which may aggravate starvation ketoacidosis.6 In conclusion, starvation should be considered as one of the causes of severe ketoacidosis in individuals with an eating disorder, even when the patient denies diet restriction.

Lactation Ketoacidosis: An Unusual Entity and a Review of the Literature.

A 31-year-old woman presented to the hospital with symptoms of nausea, malaise, and emesis. She was breastfeeding her 10-month-old infant. She was found to have severe ketoacidosis. The patient was not in diabetic ketoacidosis or alcoholic ketoacidosis; nor had she ingested any toxins. After she was admitted to the hospital, received intravenous fluids, and stopped breastfeeding, her symptoms resolved. She was found to have lactation ketoacidosis, an uncommon condition in humans. A review of all causes of ketoacidosis is presented with special emphasis on lactation ketocacidosis.

Current practice of diabetes education in children and adolescents with type 1 diabetes in Germany and Austria: analysis based on the German/Austrian DPV database.

Diabetes education of patients and/or parents is an essential part of diabetes care with effects on diabetes outcome. The objective of our study was to describe the current practice of diabetes education in Germany and Austria with regard to training frequency, patient age, migration background and diabetes therapy in a large cohort of pediatric patients with diabetes mellitus type 1 (T1DM). We analyzed data from pediatric T1DM patients with diabetes training in 2013 and complete data available for treatment year in the multicenter Diabetes Patienten Verlaufsdokumentation (DPV) registry using sas 9.4. In 2013 21 871 pediatric patients with T1DM were documented [52.4% male, age: 12.70 (9.35-15.30) yr (median (interquartile range)], diabetes duration: 3.80 (1.45-7.00) yr, migration background: 21.4%, twice daily injections: 5.5%, multiple daily injections: 52.5%, insulin-pump therapy: 42%. Of these 32.31% were trained in 2013. Younger patients and their parents were trained more intensely and more frequently as inpatients compared with older patients (0-6 vs. 6-12 and 12-18 yr: teaching units: 13.07 vs. 12.05 and 9.79; inpatient: 79% vs. 72% and 70%). There was also a difference in training frequency with regard to migration background. Severe hypoglycemia or ketoacidosis resulted in intensification of training (4.0 vs. 2.0%; 7.8 vs. 3.1%). Centre-specific education tools were used frequently alone or in combination with published, standardized education programs. Training frequency was highest in younger patients and during the first year of diabetes. Acute complications resulted in more frequent diabetes training, indicating that currently many education sessions take place in consequence to these complications.