Diabetic Coma Recovery: What You Need To Know
In people with diabetes, a diabetic coma occurs when severe levels of either high or low uncontrolled blood sugar are not corrected. If treated quickly, a person will make a rapid recovery from a diabetic coma. However, diabetic coma can be fatal or result in brain damage. It is important for people with diabetes to control their blood sugars and know what to do when their blood sugar levels are not within their target range. The severe symptoms of uncontrolled blood sugar that can come before a diabetic coma include vomiting, difficulty breathing, confusion, weakness, and dizziness. Recovery from diabetic coma If a diabetic coma is not treated within a couple of hours of it developing, it can cause irreversible brain damage. If no treatment is received, a diabetic coma will be fatal. In addition, having blood sugar levels that continue to be too low or too high can be bad for long-term health. This remains true even if they do not develop into diabetic coma. Recognizing the early signs of low or high blood sugar levels and regular monitoring can help people with diabetes keep their blood sugar levels within the healthy range. Doing so will also reduce the risk of associated complications and diabetic coma. What is diabetes? Diabetes is a long-term condition in which the body is unable to control the level of a sugar called glucose in the blood. Diabetes is caused by either a lack of insulin, the body's inability to use insulin correctly, or both. In people who don't have diabetes, insulin usually ensures that excess glucose is removed from the bloodstream. It does this by stimulating cells to absorb the glucose they need for energy from the blood. Insulin also causes any remaining glucose to be stored in the liver as a substance called glycogen. The production of insul Continue reading >>
Diabetic Ketoacidosis And Brain Function
Diabetic Ketoacidosis (DKA) is a life-threatening consequence of diabetes. DKA occurs when there is a lack of insulin in the body causing hyperglycemia. As a result of the inability of glucose to enter the cells, the body must find other means to obtain energy. As such, fat breakdown occurs resulting in the accumulation of fatty acids. The fatty acids are metabolized to ketones that cause the blood to become acidotic (pH less than7.3). Because glucose remains in the blood, there is an increase in thirst and drinking to eliminate the solute load of glucose, which also results in increased urination (polyuria and polydipsia). Thus, the combination of increased serum acidity, weight loss, polyuria, and polydipsia may lead to extreme dehydration, coma, or brain damage. Without a doubt, the most severe acute complication of DKA is cerebral edema. Many cases of new onset type 1 diabetes present DKA (15-70 percent depending on age and geographic region, according to multiple studies), hence the importance of an early diagnosis of diabetes in order to avoid potential consequences. Much research is being conducted to predict the development of severe complications of DKA, most notably on brain herniation, the swelling of the brain that causes it to push towards the spinal cord, as well as other neurological consequences. Fulminant cerebral edema, or swelling of the brain, is relatively rare and has an incidence rate of 0.5-0.9 percent. However, what about the subtler, less severe alterations in brain functions that occur after DKA? Indeed, a recent paper published in Diabetes Care 2014; 37: 1554-1562by Cameron, Scratch, Nadebaum, Northum, Koves, Jennings, Finney, Neil, Wellard, Mackay, and Inder on behalf of the DKA Brain Injury Study Group entitled "Neurological Consequences of Continue reading >>
Cerebral Edema In Diabetic Ketoacidosis: A Look Beyond Rehydration
The Journal of Clinical Endocrinology & Metabolism 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 m 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 >>
Brain Injury With Diabetes Mellitus: Evidence, Mechanisms And Treatment Implications.
Brain injury with diabetes mellitus: evidence, mechanisms and treatment implications. a Department of Neurology and Psychiatry , Assiut University Hospital , Assiut , Egypt. Expert Rev Clin Pharmacol. 2017 Apr;10(4):409-428. doi: 10.1080/17512433.2017.1293521. Epub 2017 Feb 22. Diabetes mellitus is a risk for brain injury. Brain injury is associated with acute and chronic hyperglycaemia, insulin resistance, hyperinsulinemia, diabetic ketoacidosis (DKA) and hypoglycaemic events in diabetic patients. Hyperglycemia is a cause of cognitive deterioration, low intelligent quotient, neurodegeneration, brain aging, brain atrophy and dementia. Areas covered: The current review highlights the experimental, clinical, neuroimaging and neuropathological evidence of brain injury induced by diabetes and its associated metabolic derangements. It also highlights the mechanisms of diabetes-induced brain injury. It seems that the pathogenesis of hyperglycemia-induced brain injury is complex and includes combination of vascular disease, oxidative stress, neuroinflammation, mitochondrial dysfunction, apoptosis, reduction of neurotrophic factors, acetylcholinesterase (AChE) activation, neurotransmitters' changes, impairment of brain repair processes, impairment of brain glymphatic system, accumulation of amyloid and tau phosphorylation and neurodegeneration. The potentials for prevention and treatment are also discussed. Expert commentary: We summarize the risks and the possible mechanisms of DM-induced brain injury and recommend strategies for neuroprotection and neurorestoration. Recently, a number of drugs and substances [in addition to insulin and its mimics] have shown promising potentials against diabetes-induced brain injury. These include: antioxidants, neuroinflammation inhibitors, Continue reading >>
How Does Ketoacidosis Affect The Human Brain?
Diabetic Ketoacidosis (DKA) is the body’s emergency reaction to glucose starvation in the absence of insulin. It is a disastrous reaction — in general, it makes things worse rather than better, and starts a vicious cycle of blood acidity, rising blood glucose, dehydration, and blood hyperosmolality (high concentration of dissolved stuff) that can be hard to break. One of the hardest-hit organs in DKA is the brain, due to the dehydration and acidic blood entering that sensitive organ. Severe DKA may lead to brain swelling (edema) which is life-threatening. But recent studies have shown that even a short, apparently fully-recovered stint of DKA leads to measurable brain injury. Diabetic Ketoacidosis (DKA) is a life–threatening consequence of diabetes. DKA occurs when there is a lack of insulin in the body causing hyperglycemia. As a result of the inability of glucose to enter the cells, the body must find other means to obtain energy. As such, fat breakdown occurs resulting in the accumulation of fatty acids. The fatty acids are metabolized to ketones that cause the blood to become acidotic (pH less than7.3). Because glucose remains in the blood, there is an increase in thirst and drinking to eliminate the solute load of glucose, which also results in increased urination (polyuria and polydipsia). Thus, the combination of increased serum acidity, weight loss, polyuria, and polydipsia may lead to extreme dehydration, coma, or brain damage. Without a doubt, the most severe acute complication of DKA is cerebral edema. Many cases of new onset type 1 diabetes present DKA (15-70 percent depending on age and geographic region, according to multiple studies), hence the importance of an early diagnosis of diabetes in order to avoid potential consequences. Much research is be Continue reading >>
Introduction Diabetic ketoacidosis (DKA) is a dangerous complication of diabetes caused by a lack of insulin in the body. Diabetic ketoacidosis occurs when the body is unable to use blood sugar (glucose) because there isn't enough insulin. Instead, it breaks down fat as an alternative source of fuel. This causes a build-up of a by-product called ketones. Most cases of diabetic ketoacidosis occur in people with type 1 diabetes, although it can also be a complication of type 2 diabetes. Symptoms of diabetic ketoacidosis include: passing large amounts of urine feeling very thirsty vomiting abdominal pain Seek immediate medical assistance if you have any of these symptoms and your blood sugar levels are high. Read more about the symptoms of diabetic ketoacidosis. Who is affected by diabetic ketoacidosis? Diabetic ketoacidosis is a relatively common complication in people with diabetes, particularly children and younger adults who have type 1 diabetes. Younger children under four years of age are thought to be most at risk. In about 1 in 4 cases, diabetic ketoacidosis develops in people who were previously unaware they had type 1 diabetes. Diabetic ketoacidosis accounts for around half of all diabetes-related hospital admissions in people with type 1 diabetes. Diabetic ketoacidosis triggers These include: infections and other illnesses not keeping up with recommended insulin injections Read more about potential causes of diabetic ketoacidosis. Diagnosing diabetic ketoacidosis This is a relatively straightforward process. Blood tests can be used to check your glucose levels and any chemical imbalances, such as low levels of potassium. Urine tests can be used to estimate the number of ketones in your body. Blood and urine tests can also be used to check for an underlying infec Continue reading >>
Effects Of Diabetic Ketoacidosis On Visual And Verbal Neurocognitive Function In Young Patients Presenting With New-onset Type 1 Diabetes
Go to: Abstract To evaluate the effects of diabetic ketoacidosis (DKA) on neurocognitive functions in children and adolescents presenting with new-onset type 1 diabetes. Newly diagnosed patients were divided into two groups: those with DKA and those without DKA (non-DKA). Following metabolic stabilization, the patients took a mini-mental status exam prior to undergoing a baseline battery of cognitive tests that evaluated visual and verbal cognitive tasks. Follow-up testing was performed 8-12 weeks after diagnosis. Patients completed an IQ test at follow-up. Results: There was no statistical difference between the DKA and non-DKA groups neither in alertness at baseline testing nor in an IQ test at follow-up. The DKA group had significantly lower baseline scores than the non-DKA group for the visual cognitive tasks of design recognition, design memory and the composite visual memory index (VMI). At follow-up, Design Recognition remained statistically lower in the DKA group, but the design memory and the VMI tasks returned to statistical parity between the two groups. No significant differences were found in verbal cognitive tasks at baseline or follow-up between the two groups. Direct correlations were present for the admission CO2 and the visual cognitive tasks of VMI, design memory and design recognition. Direct correlations were also present for admission pH and VMI, design memory and picture memory. Pediatric patients presenting with newly diagnosed type 1 diabetes and severe but uncomplicated DKA showed a definite trend for lower cognitive functioning when compared to the age-matched patients without DKA. Keywords: diabetic ketoacidosis, Cognition, dehydration, neuroinflammation Neurocognitive tasks. Mean (standard deviation) and median (range) of standard scores of Continue reading >>
Diabetic Ketoacidosis: Brain Morphology And Cognition (dka-cog)
The purpose of this study is to assess brain and memory changes in patients with uncontrolled diabetes (a condition called diabetic ketoacidosis (DKA)) Diabetic ketoacidosis (DKA) is a common and serious medical problem. Most cases occur when patients forget or stop insulin injections. Some patients require frequent admissions to the hospital with DKA after stopping insulin. Many patients do not know why they stop insulin therapy. The investigators will test if patients with one or more episodes of DKA have poor memory and brain changes that may lead to poor management. In this study, the investigators will perform memory testing and brain images in subjects with initial DKA episode and subjects with more than 3 episodes of DKA. The results will be compared to subjects with diabetes and no history of DKA and healthy (non-diabetic) subjects. Each subject with DKA will have an MRI and cognitive testing done shortly after hospital discharge, 1 month, and 3 months after hospital discharge. Diabetic subjects without DKA and healthy controls will only come in for a single baseline visit and have a MRI and cognitive testing done. Study Type : Observational Actual Enrollment : 45 participants Observational Model: Case-Control Time Perspective: Prospective Official Title: Acute and Long-term Neuroanatomical and Cognitive Evaluation of Adult Patients With First and Recurrent Episodes of Diabetic Ketoacidosis Study Start Date : February 2015 Primary Completion Date : October 25, 2016 Study Completion Date : October 1, 2017 Group/Cohort Healthy Controls Non-diabetic subjects Diabetics without DKA Diabetic subjects (recent(< 1 year) diagnosis of diabetes) without a history of diabetic ketoacidosis (DKA) First episode of DKA Diabetic subjects that just had their primary event of diab Continue reading >>
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 >>
Is The Brain Affected In Diabetes Mellitus?
Didi....This is a very good question because the impact of diabetes on the brain is actually overlooked. Theoretically, one can say that since diabetes affects so many organs in the body, therefore, it might affect the brain as well. Practically speaking, it has been shown that chronic hyperglycemia leads to the release of mediators that cause chronic brain inflammation, reduce blood flow and damage the cells. In fact hyperglycemia raises the risk of having dementia and depression. The chances of becoming depressed or getting dementia increases when diabetes complications develop and decreases in diabetic people with good blood sugar control. Besides, cardiovascular complications could contribute to stroke by blocking the blood flow to the brain. Another way in which diabetes can affect the brain is ketoacidosis, that occurs most likely in Type I diabetes, where the brain cannot handle the excessive amounts of ketone bodies. We must not forget that hypoglycemia, resulting from an overdose of antidiabetic drugs, leads to hypoglycemic coma. Continue reading >>
Effects Of Hyperglycemia And Effects Of Ketosis On Cerebral Perfusion, Cerebral Water Distribution, And Cerebral Metabolism
Effects of Hyperglycemia and Effects of Ketosis on Cerebral Perfusion, Cerebral Water Distribution, and Cerebral Metabolism 1Department of Pediatrics, School of Medicine, University of California, Davis, Sacramento, California 2Department of Physiology and Membrane Biology, School of Medicine, University of California, Davis, Sacramento, California Corresponding author: Nicole Glaser, [email protected] . Received 2011 Sep 15; Accepted 2012 Feb 23. Copyright 2012 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See for details. This article has been cited by other articles in PMC. Diabetic ketoacidosis (DKA) may cause brain injuries in children. The mechanisms responsible are difficult to elucidate because DKA involves multiple metabolic derangements. We aimed to determine the independent effects of hyperglycemia and ketosis on cerebral metabolism, blood flow, and water distribution. We used magnetic resonance spectroscopy to measure ratios of cerebral metabolites (ATP to inorganic phosphate [Pi], phosphocreatine [PCr] to Pi, N-acetyl aspartate [NAA] to creatine [Cr], and lactate to Cr) and diffusion-weighted imaging and perfusion-weighted imaging to assess cerebral water distribution (apparent diffusion coefficient [ADC] values) and cerebral blood flow (CBF) in three groups of juvenile rats (hyperglycemic, ketotic, and normal control). ATP-to-Pi ratio was reduced in both hyperglycemic and ketotic rats in comparison with controls. PCr-to-Pi ratio was reduced in the ketotic group, and there was a trend toward reduction in the hyperglycemic group. No significant differences were observed in NAA-to-Cr or lactate-to-Cr ratio. Cortical ADC was r Continue reading >>
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 >>
Cognitive Function In Diabetes
Cognitive deficits, that is clinically relevant problems in cognitive performance, are commonly observed in people with both type 1 (T1DM) as well as type 2 diabetes (T2DM). Both diseases are related specifically to slowing of mental processing speed, psycho-motor speed, executive functions and attention. In T2DM learning and memory problems are often noted but less so in T1DM. Evidence for changes in brain structure and functioning accompanying cognitive dysfunction is accumulating. Chronic hyperglycaemia and associated microvascular disease appear to be the most important determinants of cognitive decrements in diabetes. Hypoglycaemia and hyperglycaemia Hypoglycaemia can lead to unconsciousness, seizure, coma or even death. Mild to moderate levels of hypoglycaemia commonly affect higher-order cognitive functions. Patients may experience mood changes and difficulty with memory, planning, attention and concentration . Mental speed rapidly decreases, while accuracy remains relatively unaffected. With severe hypoglycaemia, all cognitive functions may be affected, seriously decreasing a patient’s mental capabilities. Whereas blood glucose can be quickly restored, cognitive dysfunction may take up to 4 hours or more to recover fully. Acute effects of hypoglycaemia on brain structure in diabetes are rarely reported and pre-clinical data suggest that brain damage after hypoglycaemia may be the result of reactive hyperglycaemia through overcompensation of counter-regulatory actions. In neonates without diabetes, hypoglycaemia is a common cause of brain damage, delayed development and death. The acute effect of hyperglycaemia on cognition seems relatively mild, contrary to the long-term effects, and may be associated with diabetic ketoacidosis (DKA), usually observed in ch Continue reading >>
Oxidative Damage Is Present In The Fatal Brain Edema Of Diabetic Ketoacidosis
Oxidative Damage is Present in the Fatal Brain Edema of Diabetic Ketoacidosis 1Department Pediatrics, Section of Pediatric Endocrinology, Medical College of Georgia, Augusta, Georgia, USA 2Department of Pathology, Case Western Reserve University, Cleveland, Ohio, USA 3Department of Pathology, University of Maryland, Baltimore, Maryland, USA Correspondence to: William H. Hoffman, M.D., Department Pediatrics, Medical College of Georgia, Augusta, Georgia, USA; [email protected] The publisher's final edited version of this article is available at Brain Res See other articles in PMC that cite the published article. Oxidative stress is implicated as a pathogenic factor in a spectrum of chronic diseases, notably, neurodegenerative disease. Noteworthy in this regard is that type 1 diabetes mellitus (T1DM) results in oxidative stress, leading to systemic complications of T1DM. We hypothesized that oxidative stress associated with diabetic ketoacidosis (DKA) of T1DM might have measurable brain sequelae. Consistent with this hypothesis are neurohistology and neuroradiologic studies of T1DM that suggest that oxidative insults are involved in the chronic complications of diabetic encephalopathy. To further address the role of oxidative stress in an acute setting, specifically in fatal brain edema (BE) associated with DKA, we studied neuronal localization and levels of oxidative stress markers reported to be increased in other neurodegenerative conditions. We demonstrated increased levels of 8-hydroxyguansine (8OHG), 4-hydroxynonenal (HNE) and hemeoxygenase-1 (HO-1) in the pyramidal neurons of the hippocampus of DKA BE in comparison to controls. However, in the cerebellum, only 8OHG was increased in the Purkinje cells and other cells of the molecular layer. These results indicat Continue reading >>