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 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 >>
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 >>
Management Of Diabetic Ketoacidosis
Diabetic ketoacidosis is an emergency medical condition that can be life-threatening if not treated properly. The incidence of this condition may be increasing, and a 1 to 2 percent mortality rate has stubbornly persisted since the 1970s. Diabetic ketoacidosis occurs most often in patients with type 1 diabetes (formerly called insulin-dependent diabetes mellitus); however, its occurrence in patients with type 2 diabetes (formerly called non–insulin-dependent diabetes mellitus), particularly obese black patients, is not as rare as was once thought. The management of patients with diabetic ketoacidosis includes obtaining a thorough but rapid history and performing a physical examination in an attempt to identify possible precipitating factors. The major treatment of this condition is initial rehydration (using isotonic saline) with subsequent potassium replacement and low-dose insulin therapy. The use of bicarbonate is not recommended in most patients. Cerebral edema, one of the most dire complications of diabetic ketoacidosis, occurs more commonly in children and adolescents than in adults. Continuous follow-up of patients using treatment algorithms and flow sheets can help to minimize adverse outcomes. Preventive measures include patient education and instructions for the patient to contact the physician early during an illness. Diabetic ketoacidosis is a triad of hyperglycemia, ketonemia and acidemia, each of which may be caused by other conditions (Figure 1).1 Although diabetic ketoacidosis most often occurs in patients with type 1 diabetes (formerly called insulin-dependent diabetes mellitus), more recent studies suggest that it can sometimes be the presenting condition in obese black patients with newly diagnosed type 2 diabetes (formerly called non–insulin-depe Continue reading >>
Increased Activity Of Inflammasomes As Osmosensors As Cause Of Cerebral Edema In Diabetic Ketoacidosis
Increased activity of inflammasomes as osmosensors as cause of cerebral edema in diabetic ketoacidosis Diabetic ketoacidosis (DKA) related cerebral edema (CE) is associated with a high mortality and rate of neurodisability and neurocognitive difficulties. In 54% of children with DKA there is subclinical evidence of CE on MRI studies. It is known that DKA is accompanied by a systemic inflammatory response characterized by elevated cytokine levels including interleukin-1 (IL-1) and interleukin-6. IL-1 has been linked to the pathogenesis of CE. Inflammasomes like nucleotide binding domain and leucine-rich repeat containing proteins 3 (NRLP3) are multiprotein complexes generating the active form of IL-1 in response to high glucose levels. The resulting hypothesis is that increased activity of inflammasomes as osmosensors is the cause of CE in diabetic ketoacidosis. Confirmation of the hypothesis could be achieved by correlation of IL-1 and NRLP3 levels and expression with degree of subclinical CE on MRI imaging and peripheral blood glial fibrillary acidic protein levels (a marker of brain injury). If confirmed future randomized controlled trials could use NRLP3 inhibitors and IL-1 antagonists as auxiliary treatment in DKA and measure neurocognitive outcome. NLRP, cerebral edema, systemic inflammatory response syndrome Clinically manifest cerebral edema (CE) in diabetic ketoacidosis is rare in high income countries (0 to 5.5% of cases) and significantly more common in low income countries (24 to 26% of cases) . Mortality of severe diabetic ketoacidosis (DKA) is high with more than 20% and survivors are at a significant risk of at least 27%  of permanent neurodisability. The pathogenesis of the associated CE is unclear. There is subclinical and mild, not formally diagn Continue reading >>
Cerebral Edema In Pediatric Diabetic Ketoacidosis
The purpose of this trial is to compare two different rates of fluid administration during diabetic ketoacidosis (DKA) treatment in children to determine which fluid administration rate is more beneficial for brain metabolism and for preventing or decreasing brain swelling during DKA. Cerebral edema (swelling of the brain) is the most frequent serious complication of diabetic ketoacidosis (DKA) in children. The cause of cerebral edema during DKA is not well understood. Recent studies suggest that it may result from lack of adequate blood flow to the brain during DKA, before treatment starts. Brain injury, resulting in edema, may occur before treatment because of lack of adequate blood flow to the brain and additional injury may occur when adequate blood flow is re-established during treatment (called reperfusion injury). Because additional injury may occur during treatment, it is important to understand whether the rate of administration of intravenous fluids, and, therefore, the speed of reperfusion of the brain, is related to the degree of brain swelling and injury. Most current treatment protocols indicate that intravenous fluids should be administered slowly, but it may be possible that brain injury and swelling might be lessened if adequate blood flow is established more quickly. In this study, researchers will use magnetic resonance (MR) imaging to compare two different rates of fluid administration during DKA treatment in children. The investigators will use MR imaging to measure brain swelling and metabolism at three time points—twice during treatment and once after recovery from DKA—and will compare these measurements to determine which fluid administration rate has more beneficial effects on brain metabolism and brain swelling. The study's researchers hypo Continue reading >>
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 >>
What Are The Diagnostic Criteria For Cerebral Edema In Diabetic Ketoacidosis (dka)?
What are the diagnostic criteria for cerebral edema in diabetic ketoacidosis (DKA)? Muir et al have identified diagnostic criteria for cerebral edema that include abnormal response to pain, decorticate and decerebrate posturing, cranial nerve palsies, abnormal central nervous system respiratory patterns, fluctuating level of consciousness, sustained heart rate deceleration, incontinence, and more nonspecific criteria such as vomiting, headache, lethargy, and elevated diastolic blood pressure. [ 27 ] Cerebral edema begins with mental status changes and is believed to be due partially to idiogenic osmoles, which have stabilized brain cells from shrinking while the diabetic ketoacidosis was developing. Glaser NS, Marcin JP, Wootton-Gorges SL, et al. Correlation of clinical and biochemical findings with diabetic ketoacidosis-related cerebral edema in children using magnetic resonance diffusion-weighted imaging. J Pediatr. 2008 Jun 25. [Medline] . Umpierrez GE, Jones S, Smiley D, et al. Insulin analogs versus human insulin in the treatment of patients with diabetic ketoacidosis: a randomized controlled trial. Diabetes Care. 2009 Jul. 32(7):1164-9. [Medline] . [Full Text] . Herrington WG, Nye HJ, Hammersley MS, Watkinson PJ. Are arterial and venous samples clinically equivalent for the estimation of pH, serum bicarbonate and potassium concentration in critically ill patients?. Diabet Med. 2012 Jan. 29(1):32-5. [Medline] . Mrozik LT, Yung M. Hyperchloraemic metabolic acidosis slows recovery in children with diabetic ketoacidosis: a retrospective audit. Aust Crit Care. 2009 Jun 26. [Medline] . Bowden SA, Duck MM, Hoffman RP. Young children (12 yr) with type 1 diabetes mellitus have low rate of partial remission: diabetic ketoacidosis is an important risk factor. Pediatr Diabet Continue reading >>
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Cerebral Edema In Diabetic Ketoacidosis.
Department of Endocrinology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow 226 014, U.P., India. Cerebral edema is the most important complication of diabetic ketoacidosis in children. It has a high mortality rate of 20 to 90% in different series. Twenty to 40% of survivors suffer from neurologic sequelae. The pathogenetic mechanisms are still controversial and the risk factors which are thought to predict its occurrence do not consistently correlate with cerebral edema in various studies. Prevention and recognition of early warning signs, such as decreased arousal, lethargy after initial improvement, headache, vomiting, relative bradycardia and relative hypertension, are crucial. Therapeutic guidelines to prevent cerebral edema in diabetic ketoacidosis include slow rehydration over about 48 hours, avoidance of hypotonicity and of unnecessary alkali therapy. Early recognition of cerebral edema and prompt institution of hypertonic therapy with mannitol may prevent permanent neurological sequelae. Continue reading >>
Episode 63 – Pediatric Dka
Pediatric DKA was identified as one of key diagnoses that we need to get better at managing in a massive national needs assessment conducted by the fine folks at TREKK – Translating Emergency Knowledge for Kids – one of EM Cases’ partners who’s mission is to improve the care of children in non-pediatric emergency departments across the country. You might be wondering – why was DKA singled out in this needs assessment? It turns out that kids who present to the ED in DKA without a known history of diabetes, can sometimes be tricky to diagnose, as they often present with vague symptoms. When a child does have a known history of diabetes, and the diagnosis of DKA is obvious, the challenge turns to managing severe, life-threatening DKA, so that we avoid the many potential complications of the DKA itself as well as the complications of treatment – cerebral edema being the big bad one. The approach to these patients has evolved over the years, even since I started practicing, from bolusing insulin and super aggressive fluid resuscitation to more gentle fluid management and delayed insulin drips, as examples. There are subtleties and controversies in the management of DKA when it comes to fluid management, correcting serum potassium and acidosis, preventing cerebral edema, as well as airway management for the really sick kids. In this episode we‘ll be asking our guest pediatric emergency medicine experts Dr. Sarah Reid, who you may remember from her powerhouse performance on our recent episodes on pediatric fever and sepsis, and Dr. Sarah Curtis, not only a pediatric emergency physician, but a prominent pediatric emergency researcher in Canada, about the key historical and examination pearls to help pick up this sometimes elusive diagnosis, what the value of serum Continue reading >>
Preventing A Drop In Effective Plasma Osmolality To Minimize The Likelihood Of Cerebral Edema During Treatment Of Children With Diabetic Ketoacidosis - Sciencedirect
Volume 150, Issue 5 , May 2007, Pages 467-473 Preventing a Drop in Effective Plasma Osmolality to Minimize the Likelihood of Cerebral Edema During Treatment of Children with Diabetic Ketoacidosis Author links open overlay panel Ewout J.HoornMD Get rights and content To test whether a drop in effective plasma osmolality (PEff osm; 2 plasma sodium [PNa] + plasma glucose concentrations) during therapy for diabetic ketoacidosis (DKA) is associated with an increased risk of cerebral edema (CE), and whether the development of hypernatremia to prevent a drop in the PEff osm is dangerous. This study is a retrospective comparison of a CE group (n = 12) and non-CE groups with hypernatremia (n = 44) and without hypernatremia (n = 13). The development of CE (at 6.8 1.5 hours) was associated with a drop in PEff osm from 304 5 to 290 5 mOsm/kg (P < .001). Control patients did not show this drop in PEff osm at 4 hours (1 2 and 2 2 vs 9 2 mOsm/kg; P < .01), because of a larger rise in PNa and/or a smaller drop in plasma glucose. During this period, the CE group received more near-isotonic fluids (69 9 vs 35 2 and 27 3 mL/kg; P < .001). The CE group had a higher mortality (3/12 vs 0/57; P = .003), and more neurologic sequelae (5/12 vs 1/57; P < .001). CE during therapy for DKA was associated with a drop in PEff osm. An adequate rise in PNa may be needed to prevent this drop in PEff osm. Continue reading >>
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How Can Cerebral Edema During Treatment Of Diabetic Ketoacidosis Be Avoided?
Abstract Cerebral edema during diabetic ketoacidosis (DKA) is a rare complication but it can be devastating, with significant mortality and long-term morbidity. Certain risk factors have been teased out with some large case-control studies, but more research needs to be done to make management guidelines safer. This article will discuss how DKA might be prevented from occurring in the first instance, known risk factors for cerebral edema, fluid and insulin management, the importance of careful monitoring during DKA treatment, and the importance of recognizing and acting on the earliest symptoms to prevent long-term harm. Continue reading >>
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Emdocs.net Emergency Medicine Educationa Well-grounded Myth? The Association Of Iv Fluids With Cerebral Edema In Pediatric Dka - Emdocs.net - Emergency Medicine Education
A Well-Grounded Myth? The Association of IV Fluids with Cerebral Edema in Pediatric DKA Author: Brit Long, MD (@long_brit, EM Attending Physician at SAUSHEC, USAF) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UT Southwestern Medical Center / Parkland Memorial Hospital) A 5-year-old little girl presents with vomiting, polyuria, and polydipsia. She has a history of type 1 diabetes on insulin. Her mom called her endocrinologist, who recommended they come in to the ED. Her vital signs demonstrate tachycardia and hypotension, and she appears ill. You order a VBG, urinalysis, CBC, renal function, and lactate, and while you consider your rehydration strategy, the endocrinologist calls and asks you to do maintenance therapy only. The patient looks ill, with hemodynamic abnormalities. Whats the literature behind cerebral edema (CE) and fluid rehydration in pediatric DKA? This post will evaluate this topic and more. Type 1 and 2 diabetes mellitus is a common chronic disease among children.1-5 A major complication is DKA with a 25% incidence.3-8 Almost 1/3 of patients have DKA at the time of initial diabetes diagnosis.3-7 Younger age, smaller body mass index, delayed treatment, infectious trigger, and lack of health insurance are risk factors for DKA.1,2,8 Even type 2 diabetics may experience DKA, with 5-25% of patients in DKA at time of diagnosis of type 2 diabetes.4,8,9 Insulin omission and infection are the most common sources for DKA.1,2 Pediatric DKA consists of hyperglycemia (serum glucose greater than 200 mg/dL), anion gap metabolic acidosis, and ketonemia.1,10-14 DKA is due to absolute or relative deficiency in insulin and excess counterregulatory hormones, with dehydration and electrolyte abnormalities. Rehydration with fluids, insulin, and potentia 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? 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). ~40% of initial brain imaging of kids with cerebral edema are NORMAL! Risk Factors for Developing Cerebral Edema 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: Sodium Bicarb was shown to be associated with Cerebral Edema in one study Unfortunately, this study did not adjust for illness severity. 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: Early detection and treatment is the best means to prevent brain injury and death. But, abnormal neurological signs are common in kids with DKA and they dont all need therapy. Muir et al published a Bedside Evaluation of Neuro State of Kids with DKA Abnormal motor or verbal response to pain Continue reading >>
A Rare And Lethal Complication: Cerebral Edema In The Adult Patient With Diabetic Ketoacidosis
A Rare and Lethal Complication: Cerebral Edema in the Adult Patient with Diabetic Ketoacidosis Correspondence should be addressed to Christopher W. Meaden ; [email protected] Received 20 July 2017; Revised 9 January 2018; Accepted 18 February 2018; Published 21 March 2018 Copyright 2018 Christopher W. Meaden et al. This is an open access article distributed under the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Commonly seen in the emergency department, diabetic ketoacidosis is a potentially lethal sequela of uncontrolled diabetes mellitus. In the adult population, a rare complication of diabetic ketoacidosis is cerebral edema. This case report discusses a 26-year-old male with new onset diabetes mellitus who developed cerebral edema leading to death. An unfortunate, yet common, complication of uncontrolled diabetes is diabetic ketoacidosis (DKA). A combination of elevated blood glucose in the setting of depleted insulin availability creates an acidic environment from the production of -hydroxybutyric acid and acetoacetic acid [ 1 ]. DKA has been linked to several devastating metabolic derangements including osmotic diuresis, depletion of intracellular potassium, accumulation of toxic ketoacids, and dysregulation of sodium hydrogen exchanger mechanisms [ 2 , 3 ]. A destructive consequence secondary to these abnormalities is cerebral edema (CE) that has been documented throughout the pediatric literature, but more sporadically in the adult literature. Cerebral edema results in poor outcomes with mortality occurring in 2125% of patients and neurological morbidity occurring in 1526% of patients [ 4 ]. A 26-year-old African American male, with Continue reading >>
Appropriate Therapy Can Prevent Cerebral Swelling In Diabetic Ketoacidosis
Appropriate therapy can prevent cerebral swelling in diabetic ketoacidosis (DKA) In considering the issue posed by the title, there are two aspects of fluid movement in the brain that should be emphasized before we consider the pathophysiology of DKA and its treatment. The first is a generalized response to induced hyperosmolality in the extracellular space (ECF). What are now known as osmolytes, previously called idiogenic osmols, small organic molecules that accumulate in cells. In mammals taurine and myoinositol are the principal (only?) osmolytes. These molecules diffuse out or metabolize very slowly when a return to normal osmolality has occurred. Because the brain is in a rigid box, such cell swelling will lead to increased intracranial pressure when there is continuing hyperosmolality without loss of ECF volume. The second aspect of fluid movement in and out of the brain relevant here is the nature of the capillaries through which water and solute diffuse. The brain capillaries, unlike most capillaries elsewhere in the body, have tight junctions between the cells. This anatomic feature produces the blood brain barrier. Solutes not actively transported across the membrane, which includes sodium and chloride ions, diffuse at a much slower rate than these ions diffuse across other capillaries where movement is nearly instantaneous. In the brain, equilibrium for sodium takes 6 h ( 1 ). On the other hand, diffusion of water is virtually instantaneous in the brain as elsewhere. Consider, then, what happens when an osmotic gradient between the plasma and brain fluid is created. Water moves instantly to equalize the osmotic concentrations while the dominant solutes (Na+ and Cl) move slowly. If the dilution gradient is from plasma to brain ECF, there will be an increase Continue reading >>