Cerebral Edema And Diabetic Ketoacidosis
Cerebral edema is the most feared emergent complication of pediatric diabetic ketoacidosis. Fortunately, it is relatively rare, but the rarity can lead to some confusion when it comes to its management. We recently discussed the use of mannitol and hypertonic saline for pediatric traumatic brain injury, but when should we consider these medications for the patient presenting with DKA? Cerebral Edema is a relatively rare. Incidence <1% of patients with DKA. Overall tends to occur in the newly diagnosed diabetic patient (4.3% vs 1.2%). While rare, it is a devastating complication. 1990 study showed case fatality rate was 64%. Those treated BEFORE respiratory failure had lower rate of mortality (30%). Lesson = treat early! The exact mechanism is not known… and may be varied between individual patients. Signs and Symptoms develop in: 66% within the first 7 hours of treatment (these tend to be younger). 33% within 10-24 hours of treatment. The diagnosis is clinical! ~40% of initial brain imaging of kids with cerebral edema are NORMAL! This is the area that often leads to finger pointing… most often those fingers being pointed toward the Emergency Physician who was initially caring for the kid. Much of the literature focused on interventions, but: Administration of Bicarb Sodium Bicarb was shown to be associated with Cerebral Edema in one study… Unfortunately, this study did not adjust for illness severity. Type of IV Fluids Generally, there is an absence of evidence that associates volume, tonicity, or rate change in serum glucose with Cerebral Edema development. There are cases presenting with cerebral edema prior to any therapies. Risk Factors that seem to stay consistent: Kids < 5 years of age More likely to have delayed diagnosis More severely ill at presentation S Continue reading >>
Risk Factors For Cerebral Edema In Children With Diabetic Ketoacidosis
Cerebral edema is an uncommon but devastating complication of diabetic ketoacidosis in children. Risk factors for this complication have not been clearly defined. In this multicenter study, we identified 61 children who had been hospitalized for diabetic ketoacidosis within a 15-year period and in whom cerebral edema had developed. Two additional groups of children with diabetic ketoacidosis but without cerebral edema were also identified: 181 randomly selected children and 174 children matched to those in the cerebral-edema group with respect to age at presentation, onset of diabetes (established vs. newly diagnosed disease), initial serum glucose concentration, and initial venous pH. Using logistic regression, we compared the three groups with respect to demographic characteristics and biochemical variables at presentation and compared the matched groups with respect to therapeutic interventions and changes in biochemical values during treatment. A comparison of the children in the cerebral-edema group with those in the random control group showed that cerebral edema was significantly associated with lower initial partial pressures of arterial carbon dioxide (relative risk of cerebral edema for each decrease of 7.8 mm Hg [representing 1 SD], 3.4; 95 percent confidence interval, 1.9 to 6.3; P<0.001) and higher initial serum urea nitrogen concentrations (relative risk of cerebral edema for each increase of 9 mg per deciliter [3.2 mmol per liter] [representing 1 SD], 1.7; 95 percent confidence interval, 1.2 to 2.5; P=0.003). A comparison of the children with cerebral edema with those in the matched control group also showed that cerebral edema was associated with lower partial pressures of arterial carbon dioxide and higher serum urea nitrogen concentrations. Of the ther Continue reading >>
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Treatment And Complications Of Diabetic Ketoacidosis In Children And Adolescents
INTRODUCTION Diabetic ketoacidosis (DKA) is the leading cause of morbidity and mortality in children with type 1 diabetes mellitus (T1DM), with a case fatality rate ranging from 0.15 percent to 0.31 percent [1-3]. DKA also can occur in children with type 2 DM (T2DM); this presentation is most common among youth of African-American descent [4-8]. (See "Classification of diabetes mellitus and genetic diabetic syndromes".) The management of DKA in children will be reviewed here (table 1). There is limited experience in the management and outcomes of DKA in children with T2DM, although the same principles should apply. The clinical manifestations and diagnosis of DKA in children and the pathogenesis of DKA are discussed elsewhere. (See "Clinical features and diagnosis of diabetic ketoacidosis in children and adolescents" and "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Epidemiology and pathogenesis".) DEFINITION Diabetic ketoacidosis – A consensus statement from the International Society for Pediatric and Adolescent Diabetes (ISPAD) in 2014 defined the following biochemical criteria for the diagnosis of diabetic ketoacidosis (DKA) [9]: Hyperglycemia – Blood glucose of >200 mg/dL (11 mmol/L) AND Metabolic acidosis – Venous pH <7.3 or a plasma bicarbonate <15 mEq/L (15 mmol/L) AND Continue reading >>
Pediatric Diabetic Ketoacidosis Emergency Department Care
Exenatide extended-release causes an increased incidence in thyroid C-cell tumors at clinically relevant exposures in rats compared to controls. It is unknown whether BYDUREON BCise causes thyroid C-cell tumors, including medullary thyroid carcinoma (MTC), in humans, as the human relevance of exenatide extended-release-induced rodent thyroid C-cell tumors has not been determined BYDUREON BCise is contraindicated in patients with a personal or family history of MTC or in patients with Multiple Endocrine Neoplasia syndrome type 2 (MEN 2). Counsel patients regarding the potential risk of MTC with the use of BYDUREON BCise and inform them of symptoms of thyroid tumors (eg, mass in the neck, dysphagia, dyspnea, persistent hoarseness). Routine monitoring of serum calcitonin or using thyroid ultrasound is of uncertain value for detection of MTC in patients treated with BYDUREON BCise Acute Pancreatitis including fatal and non-fatal hemorrhagic or necrotizing pancreatitis has been reported. After initiation, observe patients carefully for symptoms of pancreatitis. If suspected, discontinue promptly and do not restart if confirmed. Consider other antidiabetic therapies in patients with a history of pancreatitis Acute Kidney Injury and Impairment of Renal Function Altered renal function, including increased serum creatinine, renal impairment, worsened chronic renal failure, and acute renal failure, sometimes requiring hemodialysis and kidney transplantation have been reported. Not recommended in patients with severe renal impairment or end-stage renal disease. Use caution in patients with renal transplantation or moderate renal impairment Immunogenicity Patients may develop antibodies to exenatide. Patients with higher titer antibodies may have an attenuated HbA1c response. In cl Continue reading >>
Predictors Of Acute Complications In Children With Type 1 Diabetes
No significant age effect in boys. In girls, increasing incidencewith age (P<.001 for trend). Pairwise comparisonssubject to Bonferroni correction, ie, significant at the = .017. Figure 2. Predictors of Diabetic Ketoacidosis Relative risk estimates and the 95% confidence intervals for significantand independent predictors derived from age-stratified (<13 vs 13 years)and sex-adjusted Poisson regression with all variables simultaneously in themodel. Hb indicates hemoglobin. Figure 3. Incidence of Severe Hypoglycemia In females, decreasing incidence with age (P<.001for trend). Pairwise comparisons subject to Bonferroni correction, ie, significantat the = .017 level. Figure 4. Predictors of Severe Hypoglycemia Relative risk estimates and the 95% confidence intervals for significantand independent predictors derived from age-stratified (<13 vs 13 years)and sex-adjusted Poisson regression with all variables simultaneously in themodel. Table 1. Characteristics of Patients WithDiabetic Ketoacidosis* Predictors of Acute Complications in Children With Type 1 Diabetes ContextDiabetic ketoacidosis and severe hypoglycemia are acute complicationsof type 1 diabetes that are related, respectively, to insufficient or excessiveinsulin treatment. However, little is known about additional modifiable riskfactors. ObjectiveTo examine the incidence of ketoacidosis and severe hypoglycemia inchildren with diabetes and to determine the factors that predict these complications. Design, Setting, and ParticipantsA cohort of 1243 children from infancy to age 19 years with type 1 diabeteswho resided in the Denver, Colo, metropolitan area were followed up prospectivelyfor 3994 person-years from January 1, 1996, through December 31, 2000. Main Outcome MeasuresIncidence of ketoacidosis leading to hospi Continue reading >>
Management Of Diabetic Ketoacidosis In Children And Adolescents
Objectives After completing this article, readers should be able to: Describe the typical presentation of diabetic ketoacidosis in children. Discuss the treatment of diabetic ketoacidosis. Explain the potential complications of diabetic ketoacidosis that can occur during treatment. Introduction Diabetic ketoacidosis (DKA) represents a profound insulin-deficient state characterized by hyperglycemia (>200 mg/dL [11.1 mmol/L]) and acidosis (serum pH <7.3, bicarbonate <15 mEq/L [15 mmol/L]), along with evidence of an accumulation of ketoacids in the blood (measurable serum or urine ketones, increased anion gap). Dehydration, electrolyte loss, and hyperosmolarity contribute to the presentation and potential complications. DKA is the most common cause of death in children who have type 1 diabetes. Therefore, the best treatment of DKA is prevention through early recognition and diagnosis of diabetes in a child who has polydipsia and polyuria and through careful attention to the treatment of children who have known diabetes, particularly during illnesses. Presentation Patients who have DKA generally present with nausea and vomiting. In individuals who have no previous diagnosis of diabetes mellitus, a preceding history of polyuria, polydipsia, and weight loss usually can be elicited. With significant ketosis, patients may have a fruity breath. As the DKA becomes more severe, patients develop lethargy due to the acidosis and hyperosmolarity; in severe DKA, they may present with coma. Acidosis and ketosis cause an ileus that can lead to abdominal pain severe enough to raise concern for an acutely inflamed abdomen, and the elevation of the stress hormones epinephrine and cortisol in DKA can lead to an elevation in the white blood cell count, suggesting infection. Thus, leukocytosi Continue reading >>
Diabetic Ketoacidosis In A Pediatric Intensive Care Unit - Sciencedirect
Volume 93, Issue 2 , MarchApril 2017, Pages 179-184 Diabetic ketoacidosis in a pediatric intensive care unitCetoacidose diabtica em uma unidade de terapia intensiva peditrica Author links open overlay panel Clarice L.S.Lopes Open Access funded by Sociedade Brasileira de Pediatria To describe the characteristics of children aged 014 years diagnosed with diabetic ketoacidosis and compare the following outcomes between children with prior diagnosis of type 1 diabetes mellitus and children without prior diagnosis of type 1 diabetes mellitus length of hospital stay, severity on admission, insulin dosage, time of continuous insulin use, volume of fluids infused during treatment, and complications. A retrospective descriptive study with review of medical records of patients admitted to the pediatric intensive care unit of a referral hospital from June 2013 to July 2015. The following data regarding 52 admissions were analyzed: age, sex, weight, body surface area, signs, symptoms and severity on admission, blood gas, blood glucose, glycated hemoglobin, serum osmolarity, and index of mortality. The insulin dosage, time of continuous insulin use, volume administered in the expansion phase and in the first 24h, length of stay, and complications such as electrolyte disturbances, hypoglycemia, cerebral edema, and death were compared between the two groups. Patients without a previous diagnosis of DM1 were younger at admission, with mean age of 8.4 years (p<0.01), reported more nausea or vomiting, polydipsia and polyuria, and showed more weight loss (p<0.01). This study also observed a higher prevalence of hypokalemia (p<0.01) and longer hospital stay in this group. No differences in severity between groups were observed. The study showed that children without prior diagnosis of typ Continue reading >>
Rare Complications Of Pediatric Diabetic Ketoacidosis
Go to: CEREBRAL EDEMA Many children who present with DKA have some degree of altered mental status. Typically the altered status is due to acidosis or hyperosmolarity, although some studies show that subclinical cerebral edema occurs in the majority of patients in DKA[9,10]. Approximately 0.5%-1% of children in DKA develop frank cerebral edema[11-13]. Morbidity related to cerebral edema is approximately 13%-35% and mortality 24%-28%[12,14]. Risk factors for the development of cerebral edema during DKA include new onset T1DM, low bicarbonate, low partial pressure of CO2, and high BUN[13,15]. Conventional thinking attributes the mechanism of injury in cerebral edema to swelling from an influx of fluid into the brain[15-17]. This influx is thought to be due to the rapidly declining serum osmolarity caused by overly aggressive fluid resuscitation; however, data reveals the only treatment-related risk factor to be administration of bicarbonate[15]. The association between high fluid infusion rates and development of cerebral edema trends toward, but does not reach, statistical significance[13]. Radiographic confirmation of cerebral edema in patients with DKA prior to initiation of fluid therapy further discredits the association[13,15]. Also, many children have normal brain imaging at the onset of clinical cerebral edema and do not develop radiographic signs of edema until hours or days later, suggesting that edema is a consequence rather than the cause of injury[11]. A more plausible hypothesis is that cerebral edema is caused by cerebral hypoperfusion, which leads to cytotoxic edema (cell swelling and death) at presentation followed by vasogenic edema (breakdown of the blood brain barrier leading to capillary leakage) during treatment[9]. There is supporting evidence for t Continue reading >>
Pediatric Diabetic Ketoacidosis
Pediatric Diabetic Ketoacidosis Authors: Katia M. Lugo-Enriquez, MD, FACEP, Faculty, Florida Hospital Emergency Medicine Residency Program, Orlando, FL. Nick Passafiume, MD, Florida Hospital Emergency Medicine Residency Program, Orlando, FL. Peer Reviewer: Richard A. Brodsky, MD, Pediatric Emergency Medicine, St. Christopher's Hospital for Children, Assistant Professor, Drexel University, Philadelphia, PA. Children with diabetes, especially type 1, remain at risk for developing diabetic ketoacidosis (DKA). This may seem confounding in a modern society with such advanced medical care, but the fact remains that children who are type 1 diabetics have an incidence of DKA of 8 per 100 patient years.1 In fact, Neu and colleagues have noted in a multicenter analysis of 14,664 patients in Europe from 1995 to 2007 that there was no significant change in ketoacidosis presenting at diabetes onset in children.2 In children younger than 19 years old, DKA is the admitting diagnosis in 65% of all hospital admissions of patients with diabetes mellitus.3 This article reviews the presentation, diagnostic evaluation, treatment, and potential complications associated with pediatric DKA. — The Editor Introduction The overall mortality rate for children in DKA is not unimpressive: The range is 0.15% to 0.31%.4 Besides death, one of the most feared repercussions of DKA in children is cerebral edema, an entity that occurs approximately 1% of the time.5,6 Cerebral edema, with the exception of a few case reports in some young adults, has largely been a complication of treatment in the pediatric population, and the exact factors have yet to be completely determined. The mortality associated with cerebral edema may approach 20% to 50%, and the incidence of neurologic morbidity is significant and Continue reading >>
Diabetic Ketoacidosis
Print Overview Diabetic ketoacidosis is a serious complication of diabetes that occurs when your body produces high levels of blood acids called ketones. The condition develops when your body can't produce enough insulin. Insulin normally plays a key role in helping sugar (glucose) — a major source of energy for your muscles and other tissues — enter your cells. Without enough insulin, your body begins to break down fat as fuel. This process produces a buildup of acids in the bloodstream called ketones, eventually leading to diabetic ketoacidosis if untreated. If you have diabetes or you're at risk of diabetes, learn the warning signs of diabetic ketoacidosis — and know when to seek emergency care. Symptoms Diabetic ketoacidosis signs and symptoms often develop quickly, sometimes within 24 hours. For some, these signs and symptoms may be the first indication of having diabetes. You may notice: Excessive thirst Frequent urination Nausea and vomiting Abdominal pain Weakness or fatigue Shortness of breath Fruity-scented breath Confusion More-specific signs of diabetic ketoacidosis — which can be detected through home blood and urine testing kits — include: High blood sugar level (hyperglycemia) High ketone levels in your urine When to see a doctor If you feel ill or stressed or you've had a recent illness or injury, check your blood sugar level often. You might also try an over-the-counter urine ketones testing kit. Contact your doctor immediately if: You're vomiting and unable to tolerate food or liquid Your blood sugar level is higher than your target range and doesn't respond to home treatment Your urine ketone level is moderate or high Seek emergency care if: Your blood sugar level is consistently higher than 300 milligrams per deciliter (mg/dL), or 16.7 mill Continue reading >>
Pediatric Diabetic Ketoacidosis
Practice Essentials Diabetic ketoacidosis, in pediatric and adult cases, is a metabolic derangement caused by the absolute or relative deficiency of the anabolic hormone insulin. Together with the major complication of cerebral edema, it is the most important cause of mortality and severe morbidity in children with diabetes. Signs and symptoms Symptoms of acidosis and dehydration include the following: Symptoms of hyperglycemia, a consequence of insulin deficiency, include the following: Patients with diabetic ketoacidosis may also have the following signs and symptoms: Cerebral edema Most cases of cerebral edema occur 4-12 hours after initiation of treatment. Diagnostic criteria of cerebral edema include the following: Major criteria include the following: Minor criteria include the following: See Clinical Presentation for more detail. Laboratory studies The following lab studies are indicated in patients with diabetic ketoacidosis: Imaging studies Head computed tomography (CT) scanning - If coma is present or develops Chest radiography - If clinically indicated Electrocardiography Electrocardiography (ECG) is a useful adjunct to monitor potassium status. Characteristic changes appear with extremes of potassium status. See the images below. Consciousness Check the patient’s consciousness level hourly for up to 12 hours, especially in a young child with a first presentation of diabetes. The Glasgow coma scale is recommended for this purpose. See Workup for more detail. Management Replacement of the following is essential in the treatment of diabetic ketoacidosis: Insulin - Continuous, low-dose, intravenous (IV) insulin infusion is generally considered the safest and most effective insulin delivery method for diabetic ketoacidosis Potassium - After initial resuscitatio Continue reading >>
Cerebral Accidents In Pediatric Diabetic Ketoacidosis: Different Complications And Different Evolutions
Cerebral Accidents in Pediatric Diabetic Ketoacidosis: Different Complications and Different Evolutions Mozzillo E.a D'Amico A.b Fattorusso V.a Carotenuto B.b Buono P.a De Nitto E.a Falco M.a Franzese A. a I have read the Karger Terms and Conditions and agree. I have read the Karger Terms and Conditions and agree. Buy a Karger Article Bundle (KAB) and profit from a discount! If you would like to redeem your KAB credit, please log in . Save over 20% compared to the individual article price. Buy Cloud Access for unlimited viewing via different devices Access to all articles of the subscribed year(s) guaranteed for 5 years Unlimited re-access via Subscriber Login or MyKarger Unrestricted printing, no saving restrictions for personal use * The final prices may differ from the prices shown due to specifics of VAT rules. For additional information: Diabetic ketoacidosis (DKA) may be associated with neurologic complications: the most common is cerebral edema while the risk of venous and arterial stroke is rare. There is a pathogenetic link between DKA, hypercoagulability and stroke, whose risk is underestimated by clinicians. Our cases present a wide spectrum of cerebral accidents during DKA, the first one being diffuse cerebral edema, the second one venous stroke after 5 days of DKA resolution, while the third one multifocal edema suspected to be extrapontine myelinolysis although without electrolyte imbalance. Our cases suggest that DKA requires very accurate treatment, particularly at an early age, and it can be complicated by cerebral accidents even with appropriate medical care. Ho J, Mah JK, Pacaud D: Pediatric stroke associated with new onset type 1 diabetes mellitus: case reports and review of the literature. Pediatr Diabetes 2006;7:116-121. ISPAD Clinical Practice Co Continue reading >>
Cerebrovascular Complications Of Diabetic Ketoacidosis In Children
CLINICAL CASE REPORT Complicações cerebrovasculares da cetoacidose diabética em crianças Luis Felipe Mendonça de Siqueira Hospital das Clínicas, Universidade Federal de Minas Gerais (UFMG); Department of Pediatrics, Faculty of Medicine, UFMG, Belo Horizonte, MG, Brazil SUMMARY Neurological deterioration in children with diabetic ketoacidosis (DKA) is commonly caused by cerebral edema. However, subtle cerebral injuries including strokes should also be suspected, since children with hyperglycemia and DKA are prone to thrombosis. In this paper, a case involving a 2 month-old patient that presented cerebral edema and stroke as complications of DKA is reported. In the discussion, the literature on neurological complications of DKA in children is briefly reviewed, emphasizing the prothrombotic tendency of these patients. SUMÁRIO Alterações neurológicas em crianças com cetoacidose diabética (CAD) são comuns, sobretudo em decorrência de edema cerebral. Contudo, lesões cerebrais agudas, como acidente vascular cerebral (AVC), também devem ser investigadas, já que as crianças com hiperglicemia e cetoacidose têm maior chance de apresentar essa complicação. Neste relato, descreve-se a história de um paciente de 2 meses de idade que apresentou edema cerebral e AVC como complicações de um quadro de cetoacidose diabética. Durante a discussão, será feita uma breve revisão da literatura sobre as complicações neurológicas da CAD nos pacientes pediátricos enfatizando sua tendência pró-trombótica. INTRODUCTION Children with new onset type 1 diabetes mellitus (T1DM) frequently have diabetic ketoacidosis (DKA) as their initial presentation, a disorder that is associated with significant morbidity and mortality. In this context, neurological complications, in Continue reading >>
Childhood Ketoacidosis
Patient professional reference Professional Reference articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use. You may find one of our health articles more useful. Diabetic ketoacidosis (DKA) is the leading cause of mortality in childhood diabetes.[1]The primary cause of DKA is absolute or relative insulin deficiency: Absolute - eg, previously undiagnosed type 1 diabetes mellitus or a patient with known type 1 diabetes who does not take their insulin. Relative - stress causes a rise in counter-regulatory hormones with relative insulin deficiency. DKA can be fatal The usual causes of death are: Cerebral oedema - associated with 25% mortality (see 'Cerebral odedema', below). Hypokalaemia - which is preventable with good monitoring. Aspiration pneumonia - thus, use of a nasogastric tube in the semi-conscious or unconscious is advised. Deficiency of insulin. Rise in counter-regulatory hormones, including glucagon, cortisol, growth hormone, and catecholamines. Thus, inappropriate gluconeogenesis and liver glycogenolysis occur compounding the hyperglycaemia, which causes hyperosmolarity and ensuing polyuria, dehydration and loss of electrolytes. Accelerated catabolism from lipolysis of adipose tissue leads to increased free fatty acid circulation, which on hepatic oxidation produces the ketone bodies (acetoacetic acid and beta-hydroxybutyric acid) that cause the metabolic acidosis. A vicious circle is usually set up as vomiting usually occurs compounding the stress and dehydration; the cycle can only be broken by providing insulin and fluids; otherwise, severe acidosis occurs and can be fatal. Biochemical criteria The biochemical criteria required for a diagnosis of DKA to be made are Continue reading >>
Risk Factors For Cerebral Oedema In Children And Adolescents With Diabetic Ketoacidosis
Risk factors for cerebral oedema in children and adolescents with diabetic ketoacidosis ?Mathematical formulae have been encoded as MathML and are displayed in this HTML version using MathJax in order to improve their display. Uncheck the box to turn MathJax off. This feature requires Javascript. Click on a formula to zoom. Cerebral 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 ( < 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 probabl Continue reading >>
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