Diabetic ketoacidosis in pregnancy.

The clinical presentation of diabetic ketoacidosis (DKA) includes nausea, vomiting, thirst, polyuria, polydipsia, abdominal pain, tachypnoea, and change in mental status in cases of severe DKA. DKA is similar in pregnant and non-pregnant women, but in pregnant women it can be seen at lower serum glucose levels and symptoms may develop more rapidly. Most, but not all, cases occur in the second or third trimester.DKA results in reduction in uteroplacental blood flow due to osmotic diuresis, and also in metabolic abnormalities (maternal acidosis, hyperglycaemia, electrolyte imbalance), resulting in fetal hypoxaemia and acidosis. In fetuses with mature cardiac activity, the fetal heart rate may show minimal or absent variability, repetitive deceleration and absence of acceleration. These abnormalities in heart rate usually resolve with resolution of the DKA, which may last for several hours before normalisation.For the patient reported on here, immediate delivery based on pathological fetal heart rate would have resulted in preterm delivery and jeopardised the maternal clinical condition. However, a holistic clinical approach by the multidisciplinary team to management of the patient led to normal term delivery 5 weeks after presentation with DKA; fetal and maternal outcome were good.

Supraventricular tachycardia associated with severe diabetic ketoacidosis in a child with new-onset type 1 diabetes mellitus.

Diabetic ketoacidosis is one of the most serious and common complications of diabetes, with between 15 and 70% of new-onset type 1 diabetes mellitus worldwide presented with diabetic ketoacidosis. Supraventricular tachycardia, however, is an infrequent complication of diabetic ketoacidosis. We present the case of a child with a new-onset type 1 diabetes mellitus with supraventricular tachycardia as a complication of paediatric diabetic ketoacidosis. The patient received intravenous fluid resuscitation, insulin, and potassium supplementation and subsequently developed stable supraventricular tachycardia initially, confirmed on a 12-lead electrocardiogram despite a structurally normal heart and normal electrolytes. Vagal manoeuvers failed to achieve sinus rhythm. The patient went into respiratory distress and was intubated, for mechanical ventilation. She received one dose of adenosine with successful conversion to sinus rhythm and a heart rate decreased from 200 to 140 beats per minutes. We conclude that supraventricular tachycardia can occur as a complication of diabetic ketoacidosis, including in new-onset type 1 diabetes mellitus. Furthermore, a combination of acidosis, potassium derangement, falling magnesium, and phosphate levels may have precipitated the event. Here, we report a case of supraventricular tachycardia as a complication of paediatric diabetic ketoacidosis.

Effects of nutritional support combined with insulin therapy on serum proteins, inflammatory factors, pentraxin-3, and serum amylase levels in patients with diabetic ketoacidosis complicated with acute pancreatitis.

ABSTRACT: To explore the effects of nutritional support combined with insulin therapy on serum protein, procalcitonin (PCT), C-reactive protein (CRP), tumor necrosis factor-α (TNF-α), pentraxin-3 (PTX-3), and serum amylase (AMS) levels in patients with diabetic ketoacidosis complicated with acute pancreatitis.A total of 64 patients with diabetic ketoacidosis complicated with acute pancreatitis admitted to our hospital from January 2018 to February 2019 were enrolled in this prospective study. They were divided into the study group and the control group according to the random number table method, with 32 patients in each group. Patients in the study group were given nutritional support combined with insulin therapy, and patients in the control group were given insulin therapy.There were no significant differences in general data including age, gender, body mass index, course and type of diabetes, acute physiology and chronic health evaluation II, RANSON, CT grades between the 2 groups before treatment (all P > .05). After 7 days of treatment, the clinical efficacy of the study group was significantly higher than that of the control group (study group vs control group, 94.44% vs 75.00%, P < .05). After 7 days of treatment, the levels of prealbumin and albumin in the study group were significantly higher than those in the control group (P < .05). After 7 days of treatment, the levels of PCT, CRP, TNF-α, PTX-3, and AMS in the 2 groups were significantly lower than those before treatment (P < .05), and the levels of PCT, CRP, TNF-α, PTX-3, and AMS in the study group were significantly lower than those in the control group. After 7 days of treatment, the levels of IgG, IgM, and IgA in the 2 groups were significantly higher than those before treatment, and the levels of IgG, IgM, and IgA in the study group were significantly higher than those in the control group (P < .05).Nutritional support combined with insulin is obviously effective in the treatment of diabetic ketoacidosis complicated with acute pancreatitis, which can improve serum protein levels, reduce inflammatory response, improve immune function, and is worthy of clinical application.

Cardiovascular disease risk factor responses to a type 2 diabetes care model including nutritional ketosis induced by sustained carbohydrate restriction at 1 year: an open label, non-randomized, controlled study.

BACKGROUND: Cardiovascular disease (CVD) is a leading cause of death among adults with type 2 diabetes mellitus (T2D). We recently reported that glycemic control in patients with T2D can be significantly improved through a continuous care intervention (CCI) including nutritional ketosis. The purpose of this study was to examine CVD risk factors in this cohort. METHODS: We investigated CVD risk factors in patients with T2D who participated in a 1 year open label, non-randomized, controlled study. The CCI group (n = 262) received treatment from a health coach and medical provider. A usual care (UC) group (n = 87) was independently recruited to track customary T2D progression. Circulating biomarkers of cholesterol metabolism and inflammation, blood pressure (BP), carotid intima media thickness (cIMT), multi-factorial risk scores and medication use were examined. A significance level of P < 0.0019 ensured two-tailed significance at the 5% level when Bonferroni adjusted for multiple comparisons. RESULTS: The CCI group consisted of 262 participants (baseline mean (SD): age 54 (8) year, BMI 40.4 (8.8) kg m-2). Intention-to-treat analysis (% change) revealed the following at 1-year: total LDL-particles (LDL-P) (- 4.9%, P = 0.02), small LDL-P (- 20.8%, P = 1.2 × 10-12), LDL-P size (+ 1.1%, P = 6.0 × 10-10), ApoB (- 1.6%, P = 0.37), ApoA1 (+ 9.8%, P < 10-16), ApoB/ApoA1 ratio (- 9.5%, P = 1.9 × 10-7), triglyceride/HDL-C ratio (- 29.1%, P < 10-16), large VLDL-P (- 38.9%, P = 4.2 × 10-15), and LDL-C (+ 9.9%, P = 4.9 × 10-5). Additional effects were reductions in blood pressure, high sensitivity C-reactive protein, and white blood cell count (all P < 1 × 10-7) while cIMT was unchanged. The 10-year atherosclerotic cardiovascular disease (ASCVD) risk score decreased - 11.9% (P = 4.9 × 10-5). Antihypertensive medication use was discontinued in 11.4% of CCI participants (P = 5.3 × 10-5). The UC group of 87 participants [baseline mean (SD): age 52 (10) year, BMI 36.7 (7.2) kg m-2] showed no significant changes. After adjusting for baseline differences when comparing CCI and UC groups, significant improvements for the CCI group included small LDL-P, ApoA1, triglyceride/HDL-C ratio, HDL-C, hsCRP, and LP-IR score in addition to other biomarkers that were previously reported. The CCI group showed a greater rise in LDL-C. CONCLUSIONS: A continuous care treatment including nutritional ketosis in patients with T2D improved most biomarkers of CVD risk after 1 year. The increase in LDL-cholesterol appeared limited to the large LDL subfraction. LDL particle size increased, total LDL-P and ApoB were unchanged, and inflammation and blood pressure decreased. Trial registration Clinicaltrials.gov: NCT02519309. Registered 10 August 2015.

Supraventricular tachycardia as a complication of severe diabetic ketoacidosis in an adolescent with new-onset type 1 diabetes.

Diabetic ketoacidosis (DKA) is one of the most common causes of morbidity and mortality in new-onset type 1 diabetes (T1D). Supraventricular tachycardia (SVT), however, is a very rare complication of DKA. We present the case of a patient with new-onset T1D who presented with DKA. He received intravenous fluid resuscitation, insulin and potassium supplementation and subsequently developed SVT, confirmed on a 12-lead electrocardiograph despite a structurally normal heart. Vagal manoeuvres and adenosine failed to restore sinus rhythm, but flecainide was successful. We conclude that SVT can occur as a complication of DKA, including in new-onset T1D. Our case is the first of this phenomenon occurring in new-onset childhood diabetes, as the few prior documented cases had established diabetes. Furthermore, a combination of potassium derangement, hypophosphataemia and falling magnesium levels may have precipitated the event.

Garcinia Cambogia, Diabetic Ketoacidosis, and Pancreatitis.

[Full article available at http://rimed.org/rimedicaljournal-2017-10.asp].

Toxigenic and metabolic causes of ketosis and ketoacidotic syndromes.

Ketoacidotic syndromes are frequently encountered in acute care medicine. This article focuses on ketosis and ketoacidotic syndromes associated with intoxications, alcohol abuse, starvation, and certain dietary supplements as well as inborn errors of metabolism. Although all of these various processes are characterized by the accumulation of ketone bodies and metabolic acidosis, there are differences in the mechanisms, clinical presentations, and principles of therapy for these heterogeneous disorders. Pathophysiologic mechanisms that account for these disorders are presented, as well as guidance regarding identification and management.

[Frequency and influencing factors of ketoacidosis at diabetes onset in children and adolescents--a long-term study between 1995 and 2009]. / Häufigkeit und Einflussfaktoren der Ketoazidose bei Diabetesmanifestation im Kindes- und Jugendalter--eine Langzeitstudie von 1995 bis 2009.

BACKGROUND: Diabetic ketoacidosis (DKA) is a frequent acute complication at onset of type 1 diabetes. It is assumed that increased public awareness about diabetes symptoms may reduce DKA rate at diabetes onset. To investigate the time-dependent trend in DKA prevalence we analysed the frequency and determinants of DKA at disease onset over 15 years in pediatric patients. PATIENTS AND METHODS: The prevalence of DKA at disease onset was analysed in individuals aged ≤18 years treated for the first time from 1995-2009 within 7 days after diagnosis in pediatric centers. Simple and multiple logistic regression analysis was performed to investigate influencing factors on DKA prevalence. Change of the probability of ketoacidosis over years were modelled in the logistic regression as linear trend. RESULTS: 16 562 individuals from 170 institutions were studied with a mean age of 9.2 ± 4.2 years. DKA (pH <7.3) was present in 20.8% of patients without a significant trend between 1995 and 2009 (p=0.222). DKA prevalence was higher in children ≤5 years (26.3%) and in the age group 10-15 years (21.7%) than in individuals aged 5-10 years (16.4%) and 15-18 years (16.9%, p<0.001). Girls had DKA more often than boys (21.2% vs. 19.3%, p=0.002). DKA frequency was increased in individuals with migration background (26.5% vs. 19.2%, p<0.001). CONCLUSIONS: DKA prevalence at diabetes onset was constant at about 21% during the last 15 years. Very young children, pubertal adolescents, girls and individuals with migration background are at higher risk for DKA at diagnosis. To prevent DKA earlier diagnosis of type 1 diabetes is warranted especially in these patient groups.

Diagnostic approach to drug-screening tests for fatal diabetic ketoacidosis: forensic autopsy of a methamphetamine abuser.

To diagnose the cause of death in autopsy cases, systematic examinations, such as macroscopic, pathological, biochemical, and toxicological are important. In this case report, drug examinations also gave very useful information to diagnose the cause of death, fatal diabetic ketoacidosis (DKA). A female methamphetamine abuser in her forties was found dead lying on a hotel bed. Diagnosing her cause of death was difficult only from the macroscopic findings because there was no fatal and/or serious injury or disease. On toxicological examination, acetone was detected at a high concentration (682 microg/mL in blood, 887 microg/mL in urine) using gas chromatography (GC). Using gas chromatography-mass spectrometry (GC-MS), methamphetamine was detected in the blood, urine, hair, and visceral organs; however, these concentrations were low. At the same time, GC-MS examination revealed a high glucose peak. From the results of the biochemical examination of urine, acetoacetic acid was 1940 micromol/L, beta-hydroxybutyric acid was 14,720 micromol/L, and glucose was 4620 mg/dL. Histologically, Langerhans' islets in the pancreas were fibrotic and atrophic, and no insulin-immunoreactive cells were observed. The subsequent police investigation also revealed that she had contracted diabetes mellitus type 1; therefore, we concluded that her cause of death was DKA, due to a lack of insulin injection.

Tratamiento insulínico en régimen basal-bolos con insulina glargina en pacientes con diabetes tipo 1 con inadecuado control metabólico / Insulin treatment in basal-bolus regimen using a insulin glargine in patients with type 1 diabetes and inadequate metabolic control

El objetivo de este trabajo era evaluar la eficacia del tratamiento con múltiples dosis de insulina (MDI) utilizando insulina glargina como insulina basal y lispro como insulina prandial. Cuarenta y cinco pacientes con diabetes tipo 1 (DM1) y un control metabólico inadecuado con terapia intensiva con insulina protamina neutra de Hagedorn (NPH) e insulina rápida, fueron tratados con una dosis de insulina glargina asociada a 3 o más dosis de insulina lispro preprandial durante 5 meses. Antes y después del tratamiento, se analizaron variables clínicas, analíticas y grado de satisfacción con el tratamiento, y se efectuó una monitorización continua de glucosa durante 48 horas al final del estudio. Los resultados fueron los siguientes: con la terapia basal-bolos se observó un aumento del índice de masa corporal (24,0 ± 3,5 frente a 24,4 ± 3,4 kg/m2; p <0,05), una reducción de las necesidades de insulina (0,86 ± 0,28 frente a 0,72 ± 0,20 UI/kg/día; p <0,001) y una disminución de los episodios de hipoglucemia grave. Al mismo tiempo, un descenso significativo tanto de la glucemia basal (189 ± 78 frente a 145 ± 58 mg/dL; p= 0,005) como de los niveles de hemoglobina glucosilada (HbA1c) (8,5 ± 1,1 frente a 7,8 ± 0,8%; p= 0,001), así como una evidente mejora en el grado de satisfacción con el tratamiento. En conclusión, el tratamiento con MDI en régimen bolos-basal con insulina glargina como insulina basal reduce la glucemia basal y el nivel de HbA1c, con menores requerimientos de insulina, e induce un ligero incremento ponderal. Además, esta terapia consigue una reducción significativa de los episodios de hipoglucemia grave, con una mejora importante en el grado de satisfacción del paciente con el tratamiento (AU)

Our aim was to evaluate the efficacy of treatment with multiple daily injections (MDI) using insulin glargine as basal insulin and insulin lispro as prandial insulin. Forty-five patients with type 1 diabetes and inadequate metabolic control with intensive therapy based on NPH insulin and rapid-acting insulin were treated with insulin glargine once daily associated with 3 or more doses of preprandial lispro insulin during 5 months. Clinical and analytical variables and satisfaction with treatment were analyzed before and after treatment, and a continuous glucose monitoring was performed during 48 hours at the end of the study. An increase in body mass index (24.01 ± 3.55 versus 24.42 ± 3.38 kg/m2, p <0.05), a reduction in insulin requirements (0.86 ± 0.28 versus 0.72 ± 0.20 IU/kg/day, p <0.001) and diminution of severe hypoglycemia episodes were observed with the basal-bolus therapy. At the same time, a significant decrease of fasting plasma glucose levels (189 ± 78 versus 145 ± 58 mg/dl, p= 0.005) and HbA1c levels (8.5 ± 1.1 versus 7.8 ± 0.8%, p= 0001), as well as an improvement in the degree of satisfaction with treatment were observed. In conclusion, treatment with MDI in basalbolus regimen with insulin glargine as basal insulin reduces fasting plasma glucose and HbA1c levels, with lower insulin requirements and a slight weight increase. Furthermore, this therapy achieves a significant reduction of episodes of severe hypoglycemia with an important improvement in the degree of treatment patient satisfaction (AU)

Ketoacidosis and the hyperosmolar hyperglycemic state in adult diabetic patients. Diagnosis and treatment.

Diabetic ketoacidosis (DKA) and the hyperosmolar hyperglycemic state (HHS) are serious acute decompensations of type 1 and 2 diabetes mellitus due to various degrees of insulin deficiency and increased levels of counterregulatory hormones. They are characterized by hyperglycemia and hyperosmolarity in HHS, and by hyperglycemia and ketoacidosis in DKA with major electrolyte imbalance; both can co-exist. Precipitating factors can usually be identified. The diagnosis can usually be suspected on clinical grounds, but must be confirmed by laboratory investigation. Treatment consists of appropriate rehydration, intravenous insulin therapy and potassium supplementation. Careful monitoring of the patient's clinical and biochemical status throughout treatment is critical. Excess mortality still occurs, particularly for HHS, emphasizing the importance of patient education and regular follow-up to prevent these potentially fatal complications.

Critical care monitoring considerations for the diabetic patient.

Diabetes mellitus (DM) is a common endocrine disease encountered in the emergency and critical care setting. The diabetic Ketoacidotic (DKA) animal represents an extreme of the DM patient with regard to hyperglycemia and acid-base and electrolyte derangements. Prompt diagnosis of DKA in a critical patient and rapid initiation of appropriate therapy are necessary for a positive outcome. The steps of treatment, in order of importance, include initiation of intravenous fluid therapy, insulin therapy, electrolyte replacement, and reversal of the metabolic acidosis. The main goals of therapy--including correction of dehydration, electrolyte abnormalities and acidosis via aggressive fluid therapy with electrolyte supplementation and correction of ketoacidosis and hyperglycemia via initiation of insulin therapy--can be achieved if these steps are followed. Because of the severity of metabolic alterations in the DKA animal, frequent and careful monitoring are paramount because they will allow the clinician to tailor treatment to each case.

Metabolic emergencies.

All patients in stupor or coma should undergo blood chemistry studies, including blood gases. The anion gap and serum osmolality must be calculated in all patients. An indwelling catheter to monitor urine content and volume is essential. Electrocardiogram monitoring is indicated in all significant metabolic acidosis, especially for evaluation of intracellular potassium effect and arrhythmias. Repeated arterial monitoring of blood gases and electrolytes is essential with the use of flow sheets. Sodium lactate and Ringer's solution should never be given in an emergency care area. Large doses of insulin (100+ units intravenously) are not necessary or indicated in diabetic ketoacidosis and may be contraindicated and dangerous especially in HHNKC. Intravenous or intramuscular regular insulin after urine tests for glucose and ketones alone should not be given. Urine dilution of serum ketones is useless, and serum dilution may be grossly misleading and contraindicated: arterial studies are much more reliable.

Diabetic ketoacidosis. Reassessment of therapeutic "truths".

The diagnosis of diabetic ketoacidosis remains, as always, a bedside clinical exercise. Rapid consideration and exclusion of other conditions associated with altered consciousness that may occur in diabetics, such as lactic acidosis, hyperosmolar states, hypoglycemia, alcohol-related ketosis, and infections, should be routine. Although recent reassessment of therapy has meant more rational and specific action, close attention to the physical and laboratory responses to treatment is equally essential for a successful outcome.

Rational management of diabetic ketoacidosis.

After a definite diagnosis, rational management begins with the construction of a grid flow sheet on which can be recorded vital signs, urine sugar and acetone, blood glucose and electrolytes, arterial blood gases and treatment (fluids, insulin, potassium). Fluids correct the hyperosmolar state, sodium deficit and hypovolemia. Hypokalemia is aggravated by insulin therapy and potassium levels must be monitored chemically and with the electrocardiogram. High-dose and low-dose insulin regimens have been used. Sudden hypoglycemia must be avoided.