A Preventable Crisis People who have had diabetic ketoacidosis, or DKA, will tell you it’s worse than any flu they’ve ever had, describing an overwhelming feeling of lethargy, unquenchable thirst, and unrelenting vomiting. “It’s sort of like having molasses for blood,” says George. “Everything moves so slow, the mouth can feel so dry, and there is a cloud over your head. Just before diagnosis, when I was in high school, I would get out of a class and go to the bathroom to pee for about 10–12 minutes. Then I would head to the water fountain and begin drinking water for minutes at a time, usually until well after the next class had begun.” George, generally an upbeat person, said that while he has experienced varying degrees of DKA in his 40 years or so of having diabetes, “…at its worst, there is one reprieve from its ill feeling: Unfortunately, that is a coma.” But DKA can be more than a feeling of extreme discomfort, and it can result in more than a coma. “It has the potential to kill,” says Richard Hellman, MD, past president of the American Association of Clinical Endocrinologists. “DKA is a medical emergency. It’s the biggest medical emergency related to diabetes. It’s also the most likely time for a child with diabetes to die.” DKA occurs when there is not enough insulin in the body, resulting in high blood glucose; the person is dehydrated; and too many ketones are present in the bloodstream, making it acidic. The initial insulin deficit is most often caused by the onset of diabetes, by an illness or infection, or by not taking insulin when it is needed. Ketones are your brain’s “second-best fuel,” Hellman says, with glucose being number one. If you don’t have enough glucose in your cells to supply energy to your brain, yo Continue reading >>
Diabetic Ketoacidosis In Dogs
My dog is diabetic. He has been doing pretty well overall, but recently he became really ill. He stopped eating well, started drinking lots of water, and got really weak. His veterinarian said that he had a condition called “ketoacidosis,” and he had to spend several days in the hospital. I’m not sure I understand this disorder. Diabetic ketoacidosis is a medical emergency that occurs when there is not enough insulin in the body to control blood sugar (glucose) levels. The body can’t use glucose properly without insulin, so blood glucose levels get very high, and the body creates ketone bodies as an emergency fuel source. When these are broken down, it creates byproducts that cause the body’s acid/base balance to shift, and the body becomes more acidic (acidosis), and it can’t maintain appropriate fluid balance. The electrolyte (mineral) balance becomes disrupted which can lead to abnormal heart rhythms and abnormal muscle function. If left untreated, diabetic ketoacidosis is fatal. How could this disorder have happened? If a diabetic dog undergoes a stress event of some kind, the body secretes stress hormones that interfere with appropriate insulin activity. Examples of stress events that can lead to diabetic ketoacidosis include infection, inflammation, and heart disease. What are the signs of diabetic ketoacidosis? The signs of diabetic ketoacidosis include: Excessive thirst/drinking Increased urination Lethargy Weakness Vomiting Increased respiratory rate Decreased appetite Weight loss (unplanned) with muscle wasting Dehydration Unkempt haircoat These same clinical signs can occur with other medical conditions, so it is important for your veterinarian to perform appropriate diagnostic tests to determine if diabetic ketoacidosis in truly the issue at hand Continue reading >>
Why Can't Animals Turn Fatty Acids Into Glucose?
Animals can’t turn fatty acids into glucose because fatty acids are metabolized 2 carbons at a time into the acetyl units of acetyl-CoA, and we have no enzymes to convert acetyl-CoA into pyruvate or any other metabolite in the gluconeogenesis pathway. Essentially, as I tell my students, the pyruvate dehydrogenase reaction is crossing the Rubicon: once it’s done, you can’t go back. The oxidative decarboxylation of pyruvate is irreversible, and there is no reverse bypass in animal cells. Acetyl-CoA of course enters the Krebs cycle, which ends with oxaloacetate, which is on the gluconeogenic pathway, but the Krebs cycle starts by reacting acetyl-CoA with OAA, and thus OAA production is balanced by OAA consumption: there is no net conversion of acetyl-CoA into OAA. Plants, fungi, and some microbes do have a way to do this: a bypass in the Krebs cycle called the glyoxylate cycle. Isocitrate, instead of being oxidized to alpha-ketoglutarate, is split into succinate and glyoxylate (HC(O)-COO), by an enzyme called isocitrate lyase. The glyoxylate reacts with another acetyl-CoA to form malate, in a reaction catalyzed by malate synthase. The succinate and malate both undergo their usual reactions in the Krebs cycle, resulting in the formation of two oxaloacetates. Thus the cell achieves a net conversion of two acetyl-CoA into OAA, and the OAA can be used for gluconeogenesis. This allows, among other things, plant seeds to store energy and carbon in the form of fats, but use them to create glucose and thus cellulose for cell walls when the seed germinates into a sprout. If we had isocitrate lyase and malate synthase, we could do this trick to, and diabetics wouldn’t have to worry about ketoacidosis. But, we don’t. Edit: for the sake of accuracy, I should mention that fat Continue reading >>
Diabetic Ketoacidosis In The Pediatric Population With Type 1 Diabetes
Diabetic Ketoacidosis in the Pediatric Population with Type 1 Diabetes Abstract: Diabetic ketoacidosis (DKA) is a leading cause of morbidity and mortality in patients with type 1 diabetes (T1DM). Individuals familiar with this complication of diabetes should be able to identify the earliest signs and symptoms and act promptly to prevent further deterioration. However, even in patients with established diabetes, the rates of DKA are considerable. This chapter discusses in detail the various aspects of DKA in the pediatric population with T1DM. The prevalence and regional effects on the prevalence of DKA as well as the specific risk factors, whether disease, patient, or physician related, are reviewed. Patients with DKA experience a condition of starvation despite the abundance of metabolic substrate (i.e., glucose); the pathophysiological mechanisms responsible for the development of DKA are outlined. Next, a detailed discussion of the clinical aspects of DKA is provided. This includes the clinical findings at presentation, the approach to treatment, and potential complications. Prevention is the best method for reducing rates of DKA. Somewhat different factors apply in patients with new-onset diabetes when compared with those with established diabetes and these are reviewed. Continue reading >>
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How Do You Cure Type 2 Diabetes Naturally With Diet?
I’m a specialist practitioner in obesity and diabetes. Type 2 diabetes can be reversed through diet. Absolutely. Firstly this is what is a normal insulin reaction looks like: Insulin is manufactured in the pancreas and secreted when your blood sugar levels rise. Blood sugar needs to be not too high and not too low. Insulin’s mechanism to remove sugar from blood is to put it into cells, like your muscles. If there is an excess after blood glucose has gone into cells it is then put in the liver and further excess becomes fat. What happens with type 2 When insulin is secreted the body’s cells have ‘‘receptors’ that accept the insulin’s key that then open the doors to the cell to let the glucose in. Sadly in type 2 the receptors become resistant to the insulin key. Therefore not enough energy gets into the cell. The body has a negative feedback system. Once the cells do not get enough energy a signal is sent back to the pancreas to manufacture even more insulin. This is a vicious cycle. Insulin keeps going up and resistance keeps getting worse. A drug, called metformin works by making cells receptive again but it has limitations and eventually other drugs are needed. This is not ideal; so how can we reverse this? Well quite simply really. The crux of this scenario is that it is the sugar spikes in the blood that are causing the high levels of insulin in the first place. Certain foods cause insulin to enter the system in a fast and high volume way and some foods hardly disturb insulin at all. The insulin index is similar to the GI system and by picking foods that cause little insulin response the type 2 diabetes begins to reverse. This is a snapshot. The lower the number the lower the insulin response Sadly many government guidelines are not beneficial and larg Continue reading >>
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Diabetic Ketoacidosis ?
I am a type 1 diabetic and I have a problem that I cant seem to figure out. I have an appointment with my doctor in about a month, because they cant get me in any earlier. But what happens is I get really sick to my stomach, my blood sugar usually drops EXTREMELY fast, I get dizzy, a headache, and I always seem to yawn a lot. I have some ideas about what it might be, like ketoacidosis. But I am not entirely sure. Do you have any ideas? I would suggest that you go to your local drug store and obtain a canister of ketosticks. Check your urine for ketone. It is a very simple test. This will tell if you have ketonuria. If this is the case it is important that you see a doctor immediately. Call you doctor and tell them what is happening and you need help very quickly. If your doctor does not see you, go to an emergency room. This is a very serious situation. Take care, Wanda QUOTE posted on the "about portions'' thread: "The presence of ketones is called "ketonuria," and further dehydration and ketone build-up can result in ketoacidosis which is a medical emergency. The bottom line is that the presence of ketones in someone with type 1 diabetes shows a dangerous lack of insulin and the immediate need for more insulin. Exercise, at this time, will only burn more fat and produce more ketones. " (+ info) diabetic ketoacidosis? if you die of diabetic ketoacidosis are there warning signs before you die and when does it alert your body? and is this something that just happens to some one or is it due to the fact of foul play by the person or someone else. how is foul pay involved. if you die at the age of 40 is it required for an autopsy to be preformed There are major warning signs if diabetic ketoacidosis (DKA). Once the DKA is advanced the diabetic will vomit everything he or s Continue reading >>
Diabetic coma is a reversible form of coma found in people with diabetes mellitus. It is a medical emergency. Three different types of diabetic coma are identified: Severe low blood sugar in a diabetic person Diabetic ketoacidosis (usually type 1) advanced enough to result in unconsciousness from a combination of a severely increased blood sugar level, dehydration and shock, and exhaustion Hyperosmolar nonketotic coma (usually type 2) in which an extremely high blood sugar level and dehydration alone are sufficient to cause unconsciousness. In most medical contexts, the term diabetic coma refers to the diagnostical dilemma posed when a physician is confronted with an unconscious patient about whom nothing is known except that they have diabetes. An example might be a physician working in an emergency department who receives an unconscious patient wearing a medical identification tag saying DIABETIC. Paramedics may be called to rescue an unconscious person by friends who identify them as diabetic. Brief descriptions of the three major conditions are followed by a discussion of the diagnostic process used to distinguish among them, as well as a few other conditions which must be considered. An estimated 2 to 15 percent of diabetics will suffer from at least one episode of diabetic coma in their lifetimes as a result of severe hypoglycemia. Types Severe hypoglycemia People with type 1 diabetes mellitus who must take insulin in full replacement doses are most vulnerable to episodes of hypoglycemia. It is usually mild enough to reverse by eating or drinking carbohydrates, but blood glucose occasionally can fall fast enough and low enough to produce unconsciousness before hypoglycemia can be recognized and reversed. Hypoglycemia can be severe enough to cause un Continue reading >>
Gastrointestinal Manifestations Of Diabetic Ketoacidosis.
The evaluation of gastrointestinal symptoms in patients with diabetic acidosis frequently challenges the physician's clinical acumen. Faced with a seriously ill patient, he must judge whether the abdominal pain, nausea, or vomiting are a consequence of the metabolic decompensation, and hence likely to resolve with correction of the ketoacidosis, or if these symptoms signal a serious underlying intra-abdominal process (e.g., cholecystitis, appendicitis, etc.) which may have precipitated the development of ketoacidosis. The pathogenesis of the reversible gastrointestinal symptoms which frequently accompany diabetic acidosis has not been rigorously defined and may be multifactorial, involving metabolic, humoral, and neural processes. Careful attention to the medical history and abdominal examination greatly facilitates distinguishing patients with intra-abdominal pathology from those with reversible symptoms secondary to ketoacidosis. Similarly, the judicious use of laboratory tests (electrocardiography, blood counts, urinalysis, serum enzyme profile, and abdominal roentgenograms) materially aids in differential diagnosis. Finally, clinical suspicion of an acute abdominal process should prompt early surgical consultation and, if required, surgical intervention as the acidosis is being brought under control. Full text Full text is available as a scanned copy of the original print version. Get a printable copy (PDF file) of the complete article (527K), or click on a page image below to browse page by page. Links to PubMed are also available for Selected References. These references are in PubMed. This may not be the complete list of references from this article. Continue reading >>
How Can Diabetic Ketoacidosis Cause Cerebral Edema In Infants?
Diabetic Ketoacidosis (DKA) in and of itself does not cause cranial edema. What happens with DKA is the excess glucose in the blood changes the osmolarity of the blood, and causes fluid shift from intracelluar to extracellular. This causes the cells to shrink somewhat. Upon finding the patient in the DKA state, the teatment is insulin and IV fluids. Insulin and the hydration IV fluids reverse the DKA state, and also the osmolarity of the extracellular fluid, causing a fluid shift back into the cell. With the osmolarity reversed, the cells begin swelling—sometimes sometimes larger than before: this is what causes the edema in the cerebrum. This is particularly dangerous because the brain cells have nowhere to go, being encased within the skull. Even though infants have fontanelles and the skull has not fused solid, the extra fluid causes compression within the brain, which in turn can adversely affect the brain function. Continue reading >>
My Dog Has Acute Kidney Failure And Diabetic Ketoacidosis. Should We Put Her To Sleep?
First of all, you have my heart felt sympathies for what you are going through. I know how painful this time must be for you and your family. That decision to put your furry kid to sleep is yours and only yours to make. I am in a position to only share my experience with my own GSD's AKD. My Dash was affected by Acute Kidney disease at the age of 9 months. Within 3-4 hours of fluid therapy, our vet told us upfront that it's not working as the creatinine level had spiked from 5 at the time of reaching the vet to 9. We were proactive in asking her what can we do to save Dash. She told us that prompt dialysis is the only chance he has, no assurances / guarantee, just a chance; and directed us to the only private facility in the city where he could be given dialysis. Unfortunately, Dash couldn't be given dialysis there due to some last minute technical glitch. During this time, his creatinine had shot up to 11. Then, as the last resort, we took him to the government Veterinary hospital (which each and every one of our contact was against) as it has the only other canine dialysis unit in the city. As our luck would have it, the dialysis unit there too got stuck at the last minute. The vet there assured us she would stabilise Dash till the next morning and then have him go through dialysis. Sure enough, Dash did pull through the night and we were back the next morning for dialysis. The unit was fixed, however, Dash was found to be unfit for dialysis as his electrolyte levels had dropped substantially as well as his blood clotting was taking longer than normal. It took us almost 2 weeks to get him fit for dialysis. During this period, his creatinine had stayed above 10, fluctuating now and then; in addition, Dash had not eaten a single morsel of food in all this time. He was b Continue reading >>
Dka-induced Takotsubo Cardiomyopathy In Patient With Known Hocm
Copyright © 2017 Ayla Gordon 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. Abstract The first published case of Diabetic Ketoacidosis-induced Takotsubo cardiomyopathy was in 2009. Our patient is the 1st reported case of Diabetic Ketoacidosis- (DKA-) induced Takotsubo cardiomyopathy (TC) in a patient with known hypertrophic cardiomyopathy (HOCM) in the United States. In the literature, there are only two examples linking DKA to TC; however, this report focuses on the biochemical and physiological causes of TC in a patient with known HOCM and new-onset DKA. TC in previously diagnosed HOCM poses particular complications. With the above patient’s baseline outflow tract obstruction due to septal hypertrophy, the acute reduction in EF due to TC resulted in transient drop in brain perfusion and, therefore, syncope. 1. Introduction The most common documented cause of Takotsubo cardiomyopathy (TC) is a neurohormonal release of catecholamines. However, in this case report of a man presenting with syncope, we describe DKA as the physiological stressor leading to TC. Upon workup for this patient’s loss of consciousness, initial labs revealed a metabolic acidotic state and a glucose level of 526 mg/dL. Troponin level was 13.8 ng/mL with EKG showing ST elevations in leads V3–V6. Emergent coronary angiography demonstrated normal coronaries with a clinical picture suggesting TC. Transthoracic echo confirmed TC. DKA was controlled by day 4 of hospital stay and repeat echo on day 5 showed documented resolution of apical ballooning. The correlation is explained physiologically; DKA increases serum catecholami Continue reading >>
Diabetic Ketoacidosis (dka) - Topic Overview
Diabetic ketoacidosis (DKA) is a life-threatening condition that develops when cells in the body are unable to get the sugar (glucose) they need for energy because there is not enough insulin. When the sugar cannot get into the cells, it stays in the blood. The kidneys filter some of the sugar from the blood and remove it from the body through urine. Because the cells cannot receive sugar for energy, the body begins to break down fat and muscle for energy. When this happens, ketones, or fatty acids, are produced and enter the bloodstream, causing the chemical imbalance (metabolic acidosis) called diabetic ketoacidosis. Ketoacidosis can be caused by not getting enough insulin, having a severe infection or other illness, becoming severely dehydrated, or some combination of these things. It can occur in people who have little or no insulin in their bodies (mostly people with type 1 diabetes but it can happen with type 2 diabetes, especially children) when their blood sugar levels are high. Your blood sugar may be quite high before you notice symptoms, which include: Flushed, hot, dry skin. Feeling thirsty and urinating a lot. Drowsiness or difficulty waking up. Young children may lack interest in their normal activities. Rapid, deep breathing. A strong, fruity breath odor. Loss of appetite, belly pain, and vomiting. Confusion. Laboratory tests, including blood and urine tests, are used to confirm a diagnosis of diabetic ketoacidosis. Tests for ketones are available for home use. Keep some test strips nearby in case your blood sugar level becomes high. When ketoacidosis is severe, it must be treated in the hospital, often in an intensive care unit. Treatment involves giving insulin and fluids through your vein and closely watching certain chemicals in your blood (electrolyt Continue reading >>
Medline ® Abstracts For References 32-35
TI The use of atypical antipsychotic agents is associated with the induction of both an indolent progression to insulin-resistant diabetes and an idiosyncratic beta-cell toxicity presenting as diabetic ketoacidosis, both of which are usually reversible or improved subsequent to cessation of treatment. The underlying mechanisms are unclear at present. Nonetheless, in light of the now numerous reports on the adverse metabolic effects of these drugs, the Consensus Development Conference which met in November 2003 recommends that metabolic risks be considered when starting atypical antipsychotic drugs. Their operative checklist includes baseline screening of candidates for antipsychotic treatment, which includes personal/family history of diabetes, weight, waist circumference, blood pressure, fasting plasma glucose and fasting lipid profile, and then follow-up of these parameters. Furthermore, the health professionals, patients, family and caregivers should be aware of the signs and symptoms of diabetes, especially when acute decompensation occurs which is commensurate with diabetic ketoacidosis. We wish, through this short report, to raise the awareness of physicians treating psychiatric patients to the possibility of new-onset diabetes during therapy with atypical antipsychotic drugs and to emphasize the necessity for increased vigilance and close metabolic follow-up of these patients. Moreover, the choice of the best antipsychotic treatment for each patient should take into consideration the diabetogenic effect of the different treatment options as well the other side effects. AD Department of Medicine and Diabetes Unit, Soroka Medical Center, Faculty of Health Sciences, Beer Sheva, Israel. [email protected] TI OBJECTIVE: The purpose of the study was to determin Continue reading >>
Diabetic Ketoacidosis - Symptoms
A A A Diabetic Ketoacidosis Diabetic ketoacidosis (DKA) results from dehydration during a state of relative insulin deficiency, associated with high blood levels of sugar level and organic acids called ketones. Diabetic ketoacidosis is associated with significant disturbances of the body's chemistry, which resolve with proper therapy. Diabetic ketoacidosis usually occurs in people with type 1 (juvenile) diabetes mellitus (T1DM), but diabetic ketoacidosis can develop in any person with diabetes. Since type 1 diabetes typically starts before age 25 years, diabetic ketoacidosis is most common in this age group, but it may occur at any age. Males and females are equally affected. Diabetic ketoacidosis occurs when a person with diabetes becomes dehydrated. As the body produces a stress response, hormones (unopposed by insulin due to the insulin deficiency) begin to break down muscle, fat, and liver cells into glucose (sugar) and fatty acids for use as fuel. These hormones include glucagon, growth hormone, and adrenaline. These fatty acids are converted to ketones by a process called oxidation. The body consumes its own muscle, fat, and liver cells for fuel. In diabetic ketoacidosis, the body shifts from its normal fed metabolism (using carbohydrates for fuel) to a fasting state (using fat for fuel). The resulting increase in blood sugar occurs, because insulin is unavailable to transport sugar into cells for future use. As blood sugar levels rise, the kidneys cannot retain the extra sugar, which is dumped into the urine, thereby increasing urination and causing dehydration. Commonly, about 10% of total body fluids are lost as the patient slips into diabetic ketoacidosis. Significant loss of potassium and other salts in the excessive urination is also common. The most common Continue reading >>
The Metabolic Derangements And Treatment Of Diabetic Ketoacidosis
This article has no abstract; the first 100 words appear below. Diabetic ketoacidosis is a common illness among patients with diabetes. The exact prevalence is unknown, but in one community the rate was estimated to be 13.4 episodes per 1000 patient-years in young persons with diabetes.1 It remains a serious event, with mortality rates as high as 6 to 10 per cent.2 , 3 In children under 10 years of age, diabetic ketoacidosis accounts for 70 per cent of diabetes-related deaths.4 Death may be due to derangements that are directly attributable to ketoacidosis, to complications associated with the illness itself, or to abnormalities induced by treatment. Because a substantial percentage of deaths is . . . Supported by a grant (AM 18573) from the U.S. Public Health Service. From the Departments of Internal Medicine and Biochemistry, Southwestern Medical School, the University of Texas Health Science Center at Dallas. Address reprint requests to Dr. Foster at the University of Texas Health Science Center at Dallas, 5323 Harry Hines Blvd., Dallas, TX 75235. Continue reading >>