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What Causes Cerebral Edema In Dka?

Symptomatic Cerebral Oedema During Treatment Of Diabetic Ketoacidosis: Effect Of Adjuvant Octreotide Infusion

Symptomatic Cerebral Oedema During Treatment Of Diabetic Ketoacidosis: Effect Of Adjuvant Octreotide Infusion

Abstract A potentially lethal complication of diabetic ketoacidosis (DKA) in children is brain oedema, whether caused by DKA itself or by the therapeutic infusion of insulin and fluids. A 10-year old previously healthy boy with DKA became unconscious and apnoeic due to cerebral oedema (confirmed by abnormal EEG and CT-scan) during treatment with intravenous fluids (36 ml/h) and insulin (0.1 units/kg/h). He was intubated and artificially ventilated, without impact on EEG and CT-scan. Subsequently, adjuvant infusion of octreotide was applied (3.5 μg/kg/h), suppressing growth hormone (GH) and IGF-1 production and necessitating the insulin dose to be reduced to 0.05 - 0.025 units/kg/h. The brain oedema improved and the boy made a full recovery. Co-therapy with octreotide was associated with a favourable outcome in the present patient with DKA and cerebral oedema. Whether this could be ascribed to the effects of octreotide on the insulin requirement or on the GH/IGF-axis remains to be elucidated. Introduction Cerebral oedema is the most feared complication of DKA. The pathogenesis appears complex and is poorly understood [1]. According to a recent working hypothesis, dehydration and hypocapnia diminish cerebral perfusion, resulting in mild brain ischaemia and subsequent cytotoxic and vasogenic cerebral oedema [1]. In this context, hypoxia-induced VEGF activity may play a role [2]. Insulin treatment might also contribute, for example via its sodium-retaining effects, or by its effects on the growth hormone (GH)/insulin-like growth factor (IGF)-axis [3]. Insulin increases serum IGF-1 and decreases IGFBP-1, thereby increasing free IGF-1 activity. IGF-1 increases capillary permeability [4] and oedema formation [5, 6], probably via increasing the activity of VEGF [7, 8]. As insu Continue reading >>

Cerebral Edema In Diabetic Ketoacidosis: A Look Beyond Rehydration

Cerebral Edema In Diabetic Ketoacidosis: A Look Beyond Rehydration

Cerebral Edema in Diabetic Ketoacidosis: A Look Beyond Rehydration Department of Pediatrics University of Florida Gainesville, Florida 32610 Search for other works by this author on: The Journal of Clinical Endocrinology & Metabolism, Volume 85, Issue 2, 1 February 2000, Pages 509513, Andrew Muir; Cerebral Edema in Diabetic Ketoacidosis: A Look Beyond Rehydration, The Journal of Clinical Endocrinology & Metabolism, Volume 85, Issue 2, 1 February 2000, Pages 509513, INJUDICIOUS fluid resuscitation is frequently suggested as the cause of the cerebral edema that is the most common cause of mortality among pediatric patients with diabetic ketoacidosis (DKA) ( 1 ). The evidence, however, supports the hypothesis that neurological demise in DKA is a multifactorial process that cannot be reliably prevented by cautious rehydration protocols. Mortality and severe morbidity can, however, be reduced when healthcare providers watch vigilantly for and respond rapidly to the sentinel neurological signs and symptoms that precede, often by hours, the dramatic collapse that is typically described in these patients. Children being treated for DKA develop clinically important neurological compromise about 0.21.0% of the time ( 2 ). Subclinical neurological pathology, causing raised intracranial pressure, likely precedes the initiation of therapy in almost all cases of DKA ( 3 5 ). Intracranial hypertension has been considered to be aggravated by therapy of the DKA ( 4 , 6 , 7 ), but in keeping with the physicians perplexity about the problem, even this widely held tenet has recently been challenged ( 8 ). The pathogenic mechanism for this terrifying complication remains unknown. Hypothetical causes of cerebral edema in children with DKA must account for: 1) its occurrence (with rare excep Continue reading >>

Diabetic Ketoacidosis And Cerebral Edema.

Diabetic Ketoacidosis And Cerebral Edema.

Abstract Cerebral edema is the leading cause of death in children presenting in diabetic ketoacidosis and occurs in 0.2 to 1% of cases. The osmolar gradient caused by the high blood glucose results in water shift from the intracelluar fluid (ICF) to the extracellular fluid (ECF) space and contraction of cell volume. Correction with insulin and intravenous fluids can result in a rapid reduction in effective osmolarity, reversal of the fluid shift and the development of cerebral edema. The goals for treatment should be a combination of intravenous fluid and insulin that results in a gradual reduction of the effective osmolarity over a 36- to 48-hour period, thereby avoiding rapid expansion of the ICF compartment and brain swelling. Continue reading >>

Unusual Case Of New Onset Diabetes Mellitus Presenting With Diabetic Ketoacidosis And Cerebral Edema With Literature Review

Unusual Case Of New Onset Diabetes Mellitus Presenting With Diabetic Ketoacidosis And Cerebral Edema With Literature Review

Nitasa Sahu*, Emma Punni, Chandra Chandran and Medhat Ismail Department of Internal Medicine, St. Joseph’s Regional Medical Center, New York Medical College, Paterson, USA Citation: Sahu N, Punni E, Chandran C, Ismail M (2016) Unusual Case of New Onset Diabetes Mellitus Presenting with Diabetic Ketoacidosis and Cerebral Edema with Literature Review. J Nephrol Ther 6: 262. doi:10.4172/2161-0959.1000262 Copyright: © 2016 Sahu N, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License; which permits unrestricted use; distribution; and reproduction in any medium; provided the original author and source are credited. Visit for more related articles at Journal of Nephrology & Therapeutics Abstract Diabetic ketoacidosis (DKA) is typically treated with volume replacement (most commonly normal saline), insulin and monitored via serial chemistry and glucose lab values. Cerebral edema, a complication occurring in approximately 1% of DKA presentations in children, with a mortality of 40-90%, has no clear identifiable risk factors. While many cases have been reported in children, there are only a few cases of clinically significant cerebral edema in adults. It is postulated the underlying mechanism is similar to that in children; excessive fluid resuscitation, rapid reduction in plasma osmolarity, and/or the administration of sodium bicarbonate. We are reporting a case of a 26 year old male with no prior medical history, who presented in diabetic ketoacidosis and was treated as per the American Diabetic Association guidelines, however, deteriorated rapidly after acute complaints of headache and irritability consistent with diffuse cerebral edema. Keywords Diabetic ketoacidosis; Cerebral edema; Adult; Mortality Introduction Dia Continue reading >>

Diabetic Ketoacidosis/cerebral Edema

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 >>

Cerebral Edema In Children With Diabetic Ketoacidosis

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 And Cerebral Edema

Diabetic Ketoacidosis And Cerebral Edema

Elliot J. Krane, M.D. Departments of Pediatrics and Anesthesiology Stanford University Medical Center Introduction In 1922 Banting and Best introduced insulin into clinical practice. A decade later the first reported case of cerebral edema complicating diabetic ketoacidosis (DKA) was reported by Dillon, Riggs and Dyer writing in the pathology literature. While the syndrome of cerebral edema complicating DKA was either not seen, ignored, or was unrecognized by the medical community until 3 decades later when the complication was again reported by Young and Bradley at the Joslin Clinic, there has since been a flurry of case reports in the 1960's and 1970's and basic and clinical research from the 1970's to the 1990's leading to our present day acceptance of this as a known complication of DKA, or of the management of DKA. In fact, we now recognize that the cerebral complications of DKA (including much less frequent cerebral arterial infarctions, venous sinus thrombosis, and central nervous system infections) are the most common cause of diabetic-related death of young diabetic patients (1), accounting for 31% of deaths associated with DKA and 20% of all diabetic deaths, having surpassed aspiration, electrolyte imbalance, myocardial infarction, etc. Furthermore, diabetes mellitus remains an important cause of hospitalization of young children. The prevalence rate of diabetes continues to grow in all Western developed nations, nearly doubling every decade, resulting in 22,000 hospital admissions in children under 15 years of age for diabetes in the United States in 1994, the majority of which were due to ketoacidosis. With approximately 4 hospital admissions of children for DKA per 100,000 population per year (2), every PICU located in a major metropolitan center will conti Continue reading >>

Cerebral Edema And Diabetic Ketoacidosis

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

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 >>

Cerebral Edema - Wikipedia

Cerebral Edema - Wikipedia

Cerebral edema is excess accumulation of fluid in the intracellular or extracellular spaces of the brain . Certain changes in morphology are associated with cerebral edema: the brain becomes soft and smooth and overfills the cranial vault , gyri (ridges) become flattened, sulci (grooves) become narrowed, and ventricular cavities become compressed. Cerebral edema can result from brain trauma or from nontraumatic causes such as ischemic stroke , cancer , or brain inflammation due to meningitis or encephalitis . [1] Vasogenic edema caused by amyloid-modifying treatments, such as monoclonal antibodies , is known as ARIA-E (amyloid-related imaging abnormalities edema). The bloodbrain barrier (BBB) or the blood cerebrospinal fluid (CSF) barrier may break down, allowing fluid to accumulate in the brain's extracellular space. Altered metabolism may cause brain cells to retain water , and dilution of the blood plasma may cause excess water to move into brain cells. Vasogenic edema occurs due to a breakdown of the tight endothelial junctions that make up the bloodbrain barrier. This allows intravascular proteins and fluid to penetrate into the parenchymal extracellular space. Once plasma constituents cross the barrier, the edema spreads; this may be quite rapid and extensive. As water enters white matter, it moves extracellularly along fiber tracts and can also affect the gray matter. This type of edema may result from trauma, tumors, focal inflammation, late stages of cerebral ischemia and hypertensive encephalopathy . Mechanisms contributing to bloodbrain barrier dysfunction include physical disruption by arterial hypertension or trauma, and tumor-facilitated release of vasoactive and endothelial destructive compounds (e.g. arachidonic acid , excitatory neurotransmitters, eico Continue reading >>

Pediatric Diabetic Ketoacidosistreatment & Management

Pediatric Diabetic Ketoacidosistreatment & Management

Pediatric Diabetic KetoacidosisTreatment & Management Author: William H Lamb, MD, MBBS, FRCP(Edin), FRCP, FRCPCH; Chief Editor: Timothy E Corden, MD more... In patients with diabetic ketoacidosis, the first principals of resuscitation apply (ie, the ABCs [airway, breathing, circulation]). [ 3 ] Outcomes are best when children are closely monitored and a changing status is promptly addressed. [ 39 , 2 ] Give oxygen, although this has no effect on the respiratory drive of acidosis. Diagnose by clinical history, physical signs, and elevated blood glucose. Fluid, insulin, and electrolyte (potassium and, in select cases, bicarbonate) replacement is essential in the treatment of diabetic ketoacidosis. Early in the treatment of diabetic ketoacidosis, when blood glucose levels are very elevated, the child can continue to experience massive fluid losses and deteriorate. Strict measurement of fluid balance is essential for optimal treatment. Continuous subcutaneous insulin infusion therapy using an insulin pump should be stopped during the treatment of diabetic ketoacidosis. Children with severe acidosis (ie, pH < 7.1) or with altered consciousness should be admitted to a pediatric intensive care unit. In cases in which the occurrence of diabetic ketoacidosis signals a new diagnosis of diabetes, the process of education and support by the diabetes team should begin when the patient recovers. In cases in which diabetic ketoacidosis occurs in a child with established diabetes, explore the cause of the episode and take steps to prevent a recurrence. Following recovery from diabetic ketoacidosis, patients require subcutaneous insulin therapy. Edge JA, Roy Y, Bergomi A, et al. Conscious level in children with diabetic ketoacidosis is related to severity of acidosis and not to blood g Continue reading >>

Pathogenesis Of Cerebral Edema After Treatment Of Diabetic Ketoacidosis - Sciencedirect

Pathogenesis Of Cerebral Edema After Treatment Of Diabetic Ketoacidosis - Sciencedirect

Volume 51, Issue 4 , April 1997, Pages 1237-1244 Pathogenesis of cerebral edema after treatment of diabetic ketoacidosis Author links open overlay panel Stephen M.Silver Pathogenesis of cerebral edema after treatment of diabetic ketoacidosis. We studied the roles of acidosis, plasma osmolality, and organic osmolytes in the pathogenesis of cerebral edema in an animal model of diabetes mellitus. Normonatremic rats with streptozotocin-induced nonketotic (NKD) and ketotic (DKA) diabetes were sacrificed before or after treatment with hypotonic saline and insulin. Brains were analyzed for water, electrolyte, and organic osmolyte content. Brain water decreased by 2% in untreated DKA and NKD despite a 12% increase in plasma osmolality due to hyperglycemia. After treatment of both NKD and DKA, brain water increased equivalently by 8%. The cerebral edema that occurred after treatment was associated with decreased brain sodium content and no change in total major brain organic osmolytes in both NKD and DKA. However, brain content of the individual osmolytes glutamine and taurine increased after treatment of DKA. In a separate study, brain water and solute content of rats with DKA were compared after treatment with either hypotonic or isotonic fluid. Animals treated with isotonic fluid had significantly less cerebral edema and higher brain sodium content than those treated with hypotonic fluid. In our studies, brain swelling after treatment of DKA and NKD was primarily due to a rapid reduction of plasma glucose and osmolality, and was not caused by sodium movement into the brain. Acidosis did not appear to play a major role in the pathogenesis of cerebral edema after treatment of DKA. Continue reading >>

Aetiology Of Cerebral Oedema In Diabetic Ketoacidosis | Emergency Medicine Journal

Aetiology Of Cerebral Oedema In Diabetic Ketoacidosis | Emergency Medicine Journal

Aetiology of cerebral oedema in diabetic ketoacidosis Aetiology of cerebral oedema in diabetic ketoacidosis Department of Emergency Medicine, Royal Brisbane Hospital, Herston, Brisbane, Queensland 4029, Australia; af.brownuq.edu.au The excellent evidence based review of the emergency management of diabetic ketoacidosis (DKA) in adults by Hardern and Quinn perpetuates the premise that unnecessarily large volumes of intravenous fluids should be avoided because of the high case fatality rate of cerebral oedema. 1 This presupposes that the rate of fluid delivery is causally related to the development of cerebral oedema, which has not been proved. The large 15 year paediatric study in the USA that analysed 6977 hospitalisations for DKA found among the 61 cases of cerebral oedema (0.9%) that after multiple logistic-regression analysis with random and matched controls, the only variables statistically associated with cerebral oedema were higher initial serum urea nitrogen concentrations and lower partial pressures of carbon dioxide at presentation. 2 In addition, smaller increases in serum sodium concentration during treatment and the use of bicarbonate were also implicated. Importantly, the rate of fluid, sodium, and insulin administration were not associated with the development of cerebral oedema, nor was the initial serum glucose or its rate of change. Clearly these findings relate to patients aged 18 years or less but most occurrences of cerebral oedema in DKA are in children and adolescents, with only rare cases in adults. However, the underlying aetiology should be no different. One unifying hypothesis is that the cerebral oedema is related to cerebral vasoconstriction, brain ischaemia, and hypoxia, as hypocapnoea causing cerebral vasoconstriction and extreme dehydrati Continue reading >>

Suspected Cerebral Edema In Diabetic Ketoacidosis: Is There Still A Role For Head Ct In Treatment Decisions?*

Suspected Cerebral Edema In Diabetic Ketoacidosis: Is There Still A Role For Head Ct In Treatment Decisions?*

Objectives:Neurologic deterioration associated with cerebral edema in diabetic ketoacidosis is typically sudden in onset, progresses rapidly, and requires emergent treatment. The utility of brain imaging by head CT in decisions to treat for cerebral edema has not been previously studied. The objective of this study was to describe the characteristics of pediatric patients with diabetic ketoacidosis who develop altered mental status and evaluate the role of head CT in this cohort. Design:Retrospective analysis of clinical, biochemical, and radiologic data. Setting:Tertiary care childrens hospital (20042010). Patients:Six hundred eighty-six admissions of patients (< 26 yr) with diabetic ketoacidosis. Measurements and Main Results:Altered mental status was documented during 96 of 686 diabetic ketoacidosis admissions (14%). Compared with alert patients, those with altered mental status were younger (median, 12.0 vs 13.1 yr; p = 0.007) and more acidotic (pH, 7.04 vs 7.19; p < 0.001), with higher serum osmolality (328 vs 315 mOsm/kg; p < 0.001) and longer hospital length of stay (4.5 vs 3 d; p = 0.002). Head CT was performed during 60 of 96 diabetic ketoacidosis admissions with altered mental status (63%), 16 (27%) of which had abnormal results. Hyperosmolar therapy for cerebral edema was given during 23 of the 60 admissions (38%), during which 12 (52%) had normal head CT results, eight of these 12 (67%) after cerebral edema treatment and four (33%) before. Of the 11 admissions with abnormal head CT results that received hyperosmolar therapy, four head CT scan (36%) occurred after hyperosmolar treatment and seven (64%) before. For the 11 admissions with head CT before cerebral edema treatment, there was a median 2-hour delay between head CT and hyperosmolar therapy. Conclusi Continue reading >>

Dka And Cerebral Oedema Do We Really Know The Cause?

Dka And Cerebral Oedema Do We Really Know The Cause?

Cerebral oedema is the most feared complication in children presenting with Diabetic Ketoacidosis (DKA). It occurs in about 1% of cases but has a mortality rate of up to 90% (Waldorf J et al Diabetes Care 2006; 29:1150-9). Patients will have a decreased conscious state and may also have cranial nerve palsies, headache and/or bradycardia and hypertension. Its incidence has remained the same since it was described in 1936 and although we have clues as to what may contribute to it, and we know that some patients have subclinical cerebral oedema at presentation(Krane et al NEJM 1985;312:1147-51), we still cant predict who will get it, nor greatly affect its high rate of mortality. There are theories of causative factors, most of which are vasogenic or osmotically based, but there is really no great evidence out there. The studies are small or retrospective, or both. One theory relates to osmolytes accumulating in brain cells. These are the compounds that maintain normal cell volumes. As extracellular osmolality decreases rapidly with treatment, water flows rapidly onto these cells causing the brain to swell. Another theory relates to Na+ / H+ exchanger, such that a correction of acidosis results in Na and water passing onto the brain cells, resulting in oedema. How much has been proven to be the actual mechanism? By my reading, not much. We believe that the following increase the chance of developing cerebral oedema: Rapid change in Osmolality (2xNa + U + Glc): ie rapid decrease in Glucose and a decrease in Sodium Initial pH < 7.1. and in more recent studies (Glaser N et al NEJM 2001;344:264-269) WHAT DOES THIS MEAN IN TERMS OF TREATMENT? FLUIDS:If the patient is hypotensive and crashing then fluid resuscitation is necessary. No question about it. However, how much we give Continue reading >>

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