Diabetic Ketoacidosis Related Cerebral Edema
Diabetic Ketoacidosis Related Cerebral Edema Diabetic Ketoacidosis Related Cerebral Edema Aka: Diabetic Ketoacidosis Related Cerebral Edema, DKA related Cerebral Edema Incidence : 0.5 to 1% of Diabetic Ketoacidosis patients Younger children (<5 years old) with new onset of diabetes and longer duration of symptoms Rapid hydration has been postulated as cause Precautions regarding fluid rate and amount are standard of care in Diabetic Ketoacidosis management (see below) However large study did not show an association with fluid rate or amount V. Precautions: Children under age 5 years old with DKA Avoid large fluid boluses beyond initial 10-20 cc/kg if at all possible Avoid dropping Serum Osmolality (calc) >3 mOsms/hour Persistent vegatative state in up to one third of surviving children Aurora and Menchine in Herbert (2014) EM:Rap 14(1): 10-11 Images: Related links to external sites (from Bing) These images are a random sampling from a Bing search on the term "Diabetic Ketoacidosis Related Cerebral Edema." Click on the image (or right click) to open the source website in a new browser window. Search Bing for all related images Related Studies (from Trip Database) Open in New Window FPnotebook.com is a rapid access, point-of-care medical reference for primary care and emergency clinicians. Started in 1995, this collection now contains 6557 interlinked topic pages divided into a tree of 31 specialty books and 722 chapters. Content is updated monthly with systematic literature reviews and conferences. Although access to this website is not restricted, the information found here is intended for use by medical providers. Patients should address specific medical concerns with their physicians. This page was written by Scott Moses, MD , last revised on 12/4/2017 and last publi Continue reading >>
Original Article Population-based Study Of Incidence And Risk Factors For Cerebral Edema In Pediatric Diabetic Ketoacidosis
Objectives To determine incidence, outcomes, and risk factors for pediatric cerebral edema with diabetic ketoacidosis (CEDKA) in Canada. This was a case-control study nested within a population-based active surveillance study of CEDKA in Canada from July 1999 to June 2001. Cases are patients with DKA <16 years of age with cerebral edema. Two unmatched control subjects per case are patients with DKA without cerebral edema. Thirteen cases of CEDKA were identified over the surveillance period for an incidence rate of 0.51%; 23% died and 15% survived with neurologic sequelae. CEDKA was present at initial presentation of DKA in 19% of cases. CEDKA was associated with lower initial bicarbonate (P = .001), higher initial urea (P = .001), and higher glucose at presentation (P = .014). Although there was a trend to association with higher fluid rates and treatment with bicarbonate, these were not independent predictors. Conclusions CEDKA remains a significant problem with a high mortality rate. No association was found between the occurrence of CEDKA and treatment factors. The presence of cerebral edema before treatment of DKA and the association with severity of illness suggest that prevention of DKA is the key to avoiding this devastating complication. Continue reading >>
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Cerebral Edema: A Complication Of Dka
DKA, or diabetic ketoacidosis, is a severe life-threatening medical complication that must be treated by doctors in a hospital. DKA is a condition in which blood glucose levels have risen dangerously high due to lack of insulin and insulin resistance. Fat begins to break down in response to energy requirements leading to high ketone levels in the blood causing your blood to become too acidic. DKA sometimes leads to cerebral edema, which is brain swelling, and if left untreated, cerebral edema can cause brain damage or lead to death. Cerebral Edema: Its relationship to DKA In order to understand cerebral edema, you must understand diabetic ketoacidosis (DKA). DKA is a situation in which blood sugar levels rise to dangerous levels in response to a lack of insulin and insulin resistance. The liver keeps producing glucose, which collects in the blood. Normally, insulin will move that glucose out of the blood and into the cells that need it, but when there is insufficient insulin or significant insulin resistance, the glucose builds up to dangerous levels (severe hyperglycemia). Because the cells that need the glucose are not getting it (remember the glucose is stuck in the blood), they signal the body to produce more glucose through the breakdown of fat. The breakdown of fat results in fat components called ketones. When ketones continue to build up in your blood stream, the patient develops a condition called diabetic ketoacidosis or DKA. Symptoms include: Abdominal pain Signifant thirst Blurry vision Nausea and vomiting[1] Polyuria (Frequent urination) Polydipsia – excessive thirst that lasts for a day or more Weight loss Weakness Confusion Cold body temperature Acetone on the breath, Rapid breathing that is shallow then deep and labored– called Kussmaul’s respirati 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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Cerebral Edema In Dka
Please donate! Funds go solely to hosting and development costs that allow medical practitioners around the globe to freely access WikEM. Almost all affected patients are <20yr [2] Associated with initial bicarb level; not rate of glucose drop Overaggressive fluid resuscitation is NOT a risk factor Begins 6-12hr after onset of therapy or may begin before initiation of treatment or up to 48h afterward Many appear to be improving from their DKA before deteriorating from cerebral edema Mannitol 0.5-1gm/kg IV bolus over 20 minutes Give a repeat does if there is an inadequate response If 2 doses of mannitol are ineffective, consider 3% saline 10mL/kg over 30min Fluid restriction - decrease the IVF infusion rate by 30% Treat noncardiogenic pulmonary edema , if present Cooke & Plotnick. Management of diabetic ketoacidosis in children and adolescents. Pediatr Rev. 2008 Dec;29(12):431-5 Glaser NS, Wootton-Gorges SL, Buonocore MH, Marcin JP, Rewers A, Strain J, et al. Frequency of sub-clinical cerebral edema in children with diabetic ketoacidosis. Pediatr Diabetes. Apr 2006;7(2):75-80. Cooke & Plotnick. Management of diabetic ketoacidosis in children and adolescents. Pediatr Rev. 2008 Dec;29(12):431-5 Continue reading >>
Cerebral Edema In Children With Diabetic Ketoacidosis
Abstract Cerebral edema is the most frequent serious complication of diabetic ketoacidosis (DKA) in children, occurring in 1% to 5% of DKA episodes. The rates of mortality and permanent neurologic morbidity from this complication are high. The pathophysiologic mechanisms underlying DKA-related cerebral edema are unclear. A number of past and more recent studies have investigated biochemical and therapeutic risk factors for the development of cerebral edema. Recent studies have shown that a higher initial serum urea nitrogen concentration and lower initial partial pressure of carbon dioxide are associated with the development of cerebral edema. This and other information suggests that the pathophysiology of DKA-related cerebral edema may involve cerebral ischemia. Preview Unable to display preview. Download preview PDF. Continue reading >>
Diabetic Ketoacidosis/cerebral Edema
How can diabetic ketoacidosisrelated cerebral edema be prevented? OVERVIEW: What every practitioner needs to know Are you sure your patient has diabetic ketoacidosisrelated cerebral edema? What are the typical findings for this disease? Cerebral edema is a potentially life-threatening complication of diabetic ketoacidosis (DKA) and is responsible for the majority of diabetes-related deaths in children. Cerebral edema typically occurs after several hours of treatment with insulin and intravenous fluids but can also occur at the time of presentation of DKA before treatment is started. The risk of cerebral edema is related to the severity of acidosis, hypocapnia, and dehydration at the time of presentation of DKA. Although severe, clinically apparent cerebral edema occurs in just 1% of DKA episodes in children, numerous studies have demonstrated that mild cerebral edema, associated with only minimal or no alterations in mental status, is present in the majority of children during DKA treatment. The relationship between intravenous fluid treatment and the risk of DKA-related cerebral edema is frequently debated; however, there are no clear associations between the use of particular fluid treatment protocols and increased risk of DKA-related cerebral edema. At present, whether and how cerebral edema can be prevented is unknown. Treatment for clinically apparent cerebral edema typically involves use of hyperosmolar agents (mannitol or hypertonic saline). DKA-related cerebral edema is a clinical diagnosis. Imaging studies may be helpful but are not always definitive. The most common symptoms of DKA-related cerebral edema include mental status changes (confusion, irritability, obtundation) associated with severe headache, recurrence of vomiting, seizures, hypertension, inappro Continue reading >>
Risk Factors For Cerebral Edema In Diabetic Ketoacidosis In A Developing Country:role Of Fluid Refractory Shock.
1. Pediatr Crit Care Med. 2012 Mar;13(2):e91-6. doi: 10.1097/PCC.0b013e3182196c6d. Risk factors for cerebral edema in diabetic ketoacidosis in a developing country:role of fluid refractory shock. (1)Advanced Pediatrics Centre, Postgraduate Institute of Medical Education and Research, Sector-12, Chandigarh, India. Erratum in Pediatr Crit Care Med. 2012 May 13(3):373. Muralindharan, Jayashree [corrected toJayashree, Muralindharan].Comment in Pediatr Crit Care Med. 2012 Mar;13(2):236-7. OBJECTIVES: To study the clinical profile and risk factors of cerebral edema inchildren with diabetic ketoacidosis with specific reference to fluid refractoryshock.DESIGN: Retrospective review of medical records.SETTING: Twelve-bed pediatric intensive care unit of a teaching hospital.PATIENTS: Seventy-seven patients admitted to pediatric intensive care unit with adiagnosis of diabetic ketoacidosis over 5 yrs.INTERVENTION: Medical records were reviewed, and data with respect to patients'age, clinical features, biochemical profile (blood glucose, osmolality,electrolytes, urea, creatinine, arterial pH, PaCO(2), and HCO(3) at admission,6-12 hrs, 24 hrs, and beyond 24 hrs), cerebral edema, presence of sepsis andshock, treatment details, and primary outcome in terms of survival or death were retrieved. Patients with and without cerebral edema were compared. Variables thatwere significant on univariate analysis were entered in a multiple logisticregression analysis to determine the predictors for cerebral edema. Odds ratioand 95% confidence interval were calculated using SPSS version 15.MEASUREMENTS AND MAIN RESULTS: Mean age of the patients was 5.6 (standarddeviation, 3.8) years. Fifty-five (71.4%) patients had new-onset diabetesmellitus. Cerebral edema was seen in 20 patients (26%). Blood gluco 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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Importance Of Timing Of Risk Factors For Cerebral Oedema During Therapy For Diabetic Ketoacidosis
Cerebral oedema is a potentially devastating complication that occurs in the first day of therapy for diabetic ketoacidosis (DKA).1,2 It is commonly seen 5–15 hours after therapy begins, and there is often little warning that it might develop. Cerebral oedema should be suspected when there is an unexpected deterioration in neurological status or the persistence of a comatose state without an obvious cause. Therefore children with DKA should be admitted to a unit where they can be observed closely for a change in neurological status that includes the development of a headache or vomiting, a diminished ability to respond to questions, or worsening coma. Cerebral oedema is primarily a clinical diagnosis. The presumptive diagnosis of cerebral oedema is more secure if there is a rapid improvement in neurological status in response to intravenous administration of 3% NaCl or hypertonic mannitol. Making and acting on a clinical diagnosis should take precedence over performing a computed tomography (CT) scan because the latter might delay the implementation of emergency therapy. In fact, confirmatory changes of cerebral oedema on CT scan studies frequently do not keep pace with the clinical course, and they might not be sensitive enough to detect cerebral oedema. Moreover, care might suffer when the patient is transported to an area of the hospital where continuous monitoring may be less than ideal. Risk factors for cerebral oedema were evaluated recently in two large, carefully conducted, retrospective reviews,1,2 where 61 and 34 patients respectively with cerebral oedema were identified. Cerebral oedema occurred in slightly less than 1% of children treated for DKA—mortality rate was 21 and 24%, respectively. The risk of cerebral oedema appeared to be greater in younger an Continue reading >>
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Paediatric Diabetic Ketoacidosis
Specialist Registrar in Paediatric Intensive Care Continuing Education in Anaesthesia Critical Care & Pain, Volume 9, Issue 6, 1 December 2009, Pages 194199, Simon Steel, Shane M. Tibby; Paediatric diabetic ketoacidosis, Continuing Education in Anaesthesia Critical Care & Pain, Volume 9, Issue 6, 1 December 2009, Pages 194199, Diabetic ketoacidosis (DKA) is the leading cause of morbidity and mortality in children with diabetes. Cerebral oedema is the most common cause of death and a high index of suspicion is always required. Cerebral oedema may be exacerbated by factors related to both DKA presentation and therapy. I.V. fluid boluses should be given cautiously. Always use low-dose insulin regimes and avoid insulin boluses. Misinterpretation of acidbase abnormalities is avoided when changes in pH and base deficit are viewed in conjunction with the anion gap (the latter being a better representation of resolution of ketoacidosis). Diabetic ketoacidosis (DKA) can occur with both types 1 and 2 diabetes mellitus, 1 and is the leading cause of morbidity and mortality in children with diabetes. 2 Unlike the adult population, paediatric mortality is mainly due to the development of cerebral oedema. 1 This article will review the pathophysiology and complications of paediatric DKA and discuss the principles behind current treatment strategies. The incidence of DKA is generally higher for type 1 diabetes, both at presentation and in the setting of established disease. Studies from Europe and the USA have estimated an incidence of DKA at first diabetic presentation of 1570% for type 1 diabetes (with patients under 5 yr of age being at highest risk), and 525% for type 2. 1 , 3 It is thought that the wide variation in incidence within both sub-types is influenced by the availabili Continue reading >>
Emdocs.net Emergency Medicine Educationcerebral Edema And Diabetic Ketoacidosis - Emdocs.net - Emergency Medicine Education
Originally published at Pediatric EM Morsels on February 21, 2014.Reposted with permission. Follow Dr. Sean M. Fox on twitter @PedEMMorsels 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? 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%). The exact mechanism is not known and may be varied between individual patients. 66% within the first 7 hours of treatment (these tend to be younger). Having either 1 Diagnostic Criterion, 2 Major Criteria, or 1 Major and 2 Minor criteria lead to 92% sensitivity and 96% specificity for recognition of Cerebral Edema early enough for intervention. This does lead treating an additional 5 children who dont have Cerebral Edema for every 1 child who does. A critical MORSEL is that for every child you treat for DKA needs to have an initial thorough neuro exam including Cranial Nerves and then frequent reassessments and document it (so your colleagues who take over care for the kid can know if there has been a change)! Continue reading >>
![Laboratory Values And Treatment Associated With Dka-related Cerebral Edema [pediatrics Classics Series]](https://diabetestalk.net/images/QfegzLEdECAnhsvF.jpg)
Laboratory Values And Treatment Associated With Dka-related Cerebral Edema [pediatrics Classics Series]
Image: PD 1. Among children admitted to 1 of 10 medical centers for diabetic ketoacidosis management, elevated serum urea nitrogen concentrations and low partial pressures of carbon dioxide were associated with significant increases in risk of developing cerebral edema. 2. Lack of pronounced serum sodium rise and use of bicarbonate for treatment were also associated with significantly increased cerebral edema risk. Original Date of Publication: January 2001 Study Rundown: Among children presenting in diabetic ketoacidosis (DKA) either during an initial type 1 diabetes mellitus I (T1DM) presentation, following bodily stresses, or medication noncompliance, 1% will experience cerebral edema. At the time of this study, mortality occurred in 40-90% of these individuals, accounting for 50-60% of T1DM-related childhood deaths. However, before this study’s publication, there was limited information regarding cerebral edema risk factors among children with T1DM. Researchers found that elevated serum nitrogen concentrations and low partial pressures of carbon dioxide were associated with significantly increased risk of children hospitalized for DKA developing cerebral edema. In addition, lack of pronounced increases in serum sodium with treatment and use of bicarbonate were also associated with significantly increased risk of cerebral edema development. This study is limited by an inability to detect the possible influence of other confounders as well as to detect the potential role of variables that did not produce noticeable changes in clinical data. This was the first large, controlled study to investigate the role of cerebral edema-associated risk factors among children being treated for DKA. It was proposed that each of these factors likely contributed to the development o Continue reading >>
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. The Pediatric Emergency Medicine Collaborative Research Committee Of The American Academy Of Pediatrics.
Department of Pediatrics, University of California, Davis, School of Medicine, USA. [email protected] BACKGROUND: Cerebral edema is an uncommon but devastating complication of diabetic ketoacidosis in children. Risk factors for this complication have not been clearly defined. METHODS: 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. RESULTS: 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 Continue reading >>
