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Euglycemic Dka Pathophysiology

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What is DIABETIC KETOACIDOSIS? What does DIABETIC KETOACIDOSIS mean? DIABETIC KETOACIDOSIS meaning - DIABETIC KETOACIDOSIS definition - DIABETIC KETOACIDOSIS explanation. Source: Wikipedia.org article, adapted under https://creativecommons.org/licenses/... license. SUBSCRIBE to our Google Earth flights channel - https://www.youtube.com/channel/UC6Uu... Diabetic ketoacidosis (DKA) is a potentially life-threatening complication of diabetes mellitus. Signs and symptoms may include vomiting, abdominal pain, deep gasping breathing, increased urination, weakness, confusion, and occasionally loss of consciousness. A person's breath may develop a specific smell. Onset of symptoms is usually rapid. In some cases people may not realize they previously had diabetes. DKA happens most often in those with type 1 diabetes, but can also occur in those with other types of diabetes under certain circumstances. Triggers may include infection, not taking insulin correctly, stroke, and certain medications such as steroids. DKA results from a shortage of insulin; in response the body switches to burning fatty acids which produces acidic ketone bodies. DKA is typically diagnosed when testing finds high blood sugar, low blood pH, and ketoacids in either the blood or urine. The primary treatment of DKA is with intravenous fluids and insulin. Depending on the severity, insulin may be given intravenously or by injection under the skin. Usually potassium is also needed to prevent the development of low blood potassium. Throughout treatment blood sugar and potassium levels should be regularly checked. Antibiotics may be required in those with an underlying infection. In those with severely low blood pH, sodium bicarbonate may be given; however, its use is of unclear benefit and typically not recommended. Rates of DKA vary around the world. About 4% of people with type 1 diabetes in United Kingdom develop DKA a year, while in Malaysia the condition affects about 25% a year. DKA was first described in 1886 and, until the introduction of insulin therapy in the 1920s, it was almost universally fatal. The risk of death with adequate and timely treatment is currently around 1–4%. Up to 1% of children with DKA develop a complication known as cerebral edema. The symptoms of an episode of diabetic ketoacidosis usually evolve over a period of about 24 hours. Predominant symptoms are nausea and vomiting, pronounced thirst, excessive urine production and abdominal pain that may be severe. Those who measure their glucose levels themselves may notice hyperglycemia (high blood sugar levels). In severe DKA, breathing becomes labored and of a deep, gasping character (a state referred to as "Kussmaul respiration"). The abdomen may be tender to the point that an acute abdomen may be suspected, such as acute pancreatitis, appendicitis or gastrointestinal perforation. Coffee ground vomiting (vomiting of altered blood) occurs in a minority of people; this tends to originate from erosion of the esophagus. In severe DKA, there may be confusion, lethargy, stupor or even coma (a marked decrease in the level of consciousness). On physical examination there is usually clinical evidence of dehydration, such as a dry mouth and decreased skin turgor. If the dehydration is profound enough to cause a decrease in the circulating blood volume, tachycardia (a fast heart rate) and low blood pressure may be observed. Often, a "ketotic" odor is present, which is often described as "fruity", often compared to the smell of pear drops whose scent is a ketone. If Kussmaul respiration is present, this is reflected in an increased respiratory rate.....

Euglycemic Diabetic Ketoacidosis: An Easily Missed Diagnosis

SESSION TITLE: Critical Care Student/Resident Case Report Posters I SESSION TYPE: Student/Resident Case Report Poster INTRODUCTION: A 47 year-old woman with type 1 diabetes presented with euglycemic diabetic ketoacidosis (DKA) that initially went undiagnosed. Recognition and treatment with insulin resulted in rapid resolution of her clinical condition. CASE PRESENTATION: A 47 year-old woman presented to our hospital with four days of fever, abdominal pain, diarrhea, nausea, vomiting, lethargy and malaise. She had a history of type 1 diabetes mellitus managed with an insulin pump. Her blood pressure was 88/51. She was disoriented with a diffusely tender but soft abdomen. Laboratory studies revealed blood glucose of 109 mg/dL, bicarbonate of 15 mmol/L, anion gap of 27 mmol/L, lactic acid of 2.4 mmol/L, and a bandemia of 11%. Rapid flu test was positive. She was admitted to the intensive care unit, resuscitated with intravenous fluid, and started on oseltamivir, cefepime and vancomycin. Hemodialysis was initiated soon thereafter. The patient received no insulin due to her euglycemia. Influenza A was detected by PCR on the second hospital day and antibiotics were discontinued. Her gast Continue reading >>

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Popular Questions

  1. BalsakianMcGiggles

    Hey guys and gals,
    Is there any standard way of getting yourself back into ketosis after eating horribly after one or two days?
    Basically, I got drunk off a few whiskey and diets last night and drunkenly ended up eating a huge bag of M&M's. Fast forward to this morning and I can feel my transgressions. Y.Y
    I'm assuming the answer just stick to the diet, but I didn't know if there was a way of eating extra lean to kick myself back into the swing of things faster? Any sort sort of routine you guys use that helps you get back on track?

  2. anbeav

    Resume keto, you'll be in ketosis within 24 hours. No need to overcompensate, just resume the program as usual

  3. TactfulEver

    If you gained weight, it's probably mostly water weight. Don't fret too much, and just get back to the diet as normal.

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Several metals, including iron, cobalt, copper and zinc, are naturally present in living organisms and play essential roles in a wide range of biological processes. In addition, some metal complexes have shown to be very successful therapeutic and diagnostic agents. Examples of these are platinum-based anticancer drugs, used in chemotherapy since the 1970s, and gadolinium-based MRI contrast agents for medical imaging. For several years Ramon Vilar and his team have been studying the chemistry of metal complexes in living organisms with the aim of developing new metal-based drugs as well as gaining a better molecular understanding of biological processes. They have a particular interest in studying how novel metal complexes interact with selected enzymes and DNA. For more information please visit http://www3.imperial.ac.uk/newsandeve...

Euglycemic Diabetic Ketoacidosis: A Diagnostic And Therapeutic Dilemma

Euglycemic diabetic ketoacidosis: a diagnostic and therapeutic dilemma 1Department of Internal Medicine, Memorial Hospital of Martinsville and Henry County, Martinsville, Virginia, USA, 2Texas Tech University Health Sciences Center, El Paso, Texas, USA, 3Senior Research Associate, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA, 4Department of Pharmacology, St Johns Medical College, Bangalore, India, Received 2017 Jul 18; Accepted 2017 Aug 4. This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License . Euglycemic diabetic ketoacidosis (EDKA) is a clinical triad comprising increased anion gap metabolic acidosis, ketonemia or ketonuria and normal blood glucose levels <200 mg/dL. This condition is a diagnostic challenge as euglycemia masquerades the underlying diabetic ketoacidosis. Thus, a high clinical suspicion is warranted, and other diagnosis ruled out. Here, we present two patients on regular insulin treatment who were admitted with a diagnosis of EDKA. The first patient had insulin pump failure and the second patient had urinary tract infection and nausea, thereby resulting in starvation. Both Continue reading >>

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  1. Steve Rapaport

    Correlation isn't causation, so the question's presupposition of high blood sugar 'resulting' in diabetic coma is wrong. They both result from common causes.
    Diabetic coma (advanced diabetic ketoacidosis or DKA) is not the result of high blood sugar, but of low insulin and water levels. Low insulin levels lead to high blood sugar AND to ketoacidosis. Hence there's no minimum blood sugar level to watch for (though there may be for a given individual).
    The best way to avoid DKA is to keep insulin levels steady in the bloodstream, keep well hydrated, and keep small amounts of food in the system at all times.
    DKA is a result of the body demanding sugar for fuel, and being denied it through lack of insulin. The body burns fat instead, which produces ketone bodies as a byproduct. The ketones build up in blood, making it acid and highly concentrated. Concentrated blood sucks water out of cells by osmosis. Dehydration makes this worse. The ketones signal the liver that glucose is desperately needed, so it dumps stored glucose to help out, but in the absence of insulin this just makes things worse -- now the blood is full of ketones AND glucose, and even more highly concentrated. Both of these conditions will get worse until fast-acting insulin and missing electrolytes are added in carefully controlled doses, including a drip-feed for hydration and frequent recheck and adjustment of all those values.

  2. Suhail Malhotra

    First we must know that there are 2 types of diabetes.
    IDDM(insulin dependent diabetes mellitus) aka Type 1
    NIDDM( non insulin dependent diabetes mellitus) aka Type 2.
    Type 1 is due to loss of insulin secretion by pancreas as in destruction of pancreas.
    Type 2 is due to insulin resistance that is insulin secretion is ok but body cells don't respond to it.
    Now the comas in these two types are different to the extent that they are named differently.
    The coma of type 1 is called the DKA(diabetic ketoacidosis) and that of type 2 is HONK( hyperosmotic non ketotic coma) now known as HHS(hyperglycemic hyperosmolar state).
    DKA occurs in type 1 diabetes or situations simulating type 1 mechanism like when a patient forgets to take his dose of insulin or in states when patient is regular with insulin but the body needs more than normal as in cases of surgery or illness or pregnancy.
    Blood glucose ranges in DKA from 250 to 600 mg/dl( 13 to 33 mmol/l) with increased ketones in blood which being acidic drive the blood ph to acidic levels ( <7.3). Symptoms include vomiting,increased urination, increased thirst, abdominal pain,increased rate of respiration(Kussumaul breathing) and in the end coma.
    HONK or HHS is caused by type 2 diabetes or situations similar to it like relative insulin deficiency combined with inadequate fluid intake and often precipitated in patients with type2 DM and a concurrent illness.
    Blood glucose ranges from 600 to 1200 mg/dl (33 to 66 mmol/l). The blood ph is normal (>=7.3) as ketones are absent. Patient is lethargic with increased thirst and increased urination leading to coma.
    Symptoms absent in HONK are nausea, vomiting, abdominal pain and increased rate of respiration which were very much a part of DKA.

  3. Jae Won Joh

    If you are asking what blood sugar levels are commonly seen in diabetic coma[1], there is a very wide range. Patients naive to the condition typically present with blood glucoses around the 300s, while those with chronic poorly-managed diabetes can present with blood glucoses over 1000.
    [1] As Steve Rapaport already pointed out in his answer, the high glucose level is not, in and of itself, the problem.

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What is KETOACIDOSIS? What does KETOACIDOSIS mean? KETOACIDOSIS meaning - KETOACIDOSIS definition - KETOACIDOSIS explanation. Source: Wikipedia.org article, adapted under https://creativecommons.org/licenses/... license. SUBSCRIBE to our Google Earth flights channel - https://www.youtube.com/channel/UC6Uu... Ketoacidosis is a metabolic state associated with high concentrations of ketone bodies, formed by the breakdown of fatty acids and the deamination of amino acids. The two common ketones produced in humans are acetoacetic acid and ß-hydroxybutyrate. Ketoacidosis is a pathological metabolic state marked by extreme and uncontrolled ketosis. In ketoacidosis, the body fails to adequately regulate ketone production causing such a severe accumulation of keto acids that the pH of the blood is substantially decreased. In extreme cases ketoacidosis can be fatal. Ketoacidosis is most common in untreated type 1 diabetes mellitus, when the liver breaks down fat and proteins in response to a perceived need for respiratory substrate. Prolonged alcoholism may lead to alcoholic ketoacidosis. Ketoacidosis can be smelled on a person's breath. This is due to acetone, a direct by-product of the spontaneous decomposition of acetoacetic acid. It is often described as smelling like fruit or nail polish remover. Ketosis may also smell, but the odor is usually more subtle due to lower concentrations of acetone. Treatment consists most simply of correcting blood sugar and insulin levels, which will halt ketone production. If the severity of the case warrants more aggressive measures, intravenous sodium bicarbonate infusion can be given to raise blood pH back to an acceptable range. However, serious caution must be exercised with IV sodium bicarbonate to avoid the risk of equally life-threatening hypernatremia. Three common causes of ketoacidosis are alcohol, starvation, and diabetes, resulting in alcoholic ketoacidosis, starvation ketoacidosis, and diabetic ketoacidosis respectively. In diabetic ketoacidosis, a high concentration of ketone bodies is usually accompanied by insulin deficiency, hyperglycemia, and dehydration. Particularly in type 1 diabetics the lack of insulin in the bloodstream prevents glucose absorption, thereby inhibiting the production of oxaloacetate (a crucial molecule for processing Acetyl-CoA, the product of beta-oxidation of fatty acids, in the Krebs cycle) through reduced levels of pyruvate (a byproduct of glycolysis), and can cause unchecked ketone body production (through fatty acid metabolism) potentially leading to dangerous glucose and ketone levels in the blood. Hyperglycemia results in glucose overloading the kidneys and spilling into the urine (transport maximum for glucose is exceeded). Dehydration results following the osmotic movement of water into urine (Osmotic diuresis), exacerbating the acidosis. In alcoholic ketoacidosis, alcohol causes dehydration and blocks the first step of gluconeogenesis by depleting oxaloacetate. The body is unable to synthesize enough glucose to meet its needs, thus creating an energy crisis resulting in fatty acid metabolism, and ketone body formation.

Euglycemic Diabetic Ketoacidosis

Abstract Introduction: Diabetic ketoacidosis (DKA) is one of the most serious complications of diabetes. It is characterised by the triad of hyperglycemia (blood sugar >250 mg/dl), metabolic acidosis (arterial pH <7.3 and serum bicarbonate <18 mEq/L) and ketosis. Rarely these patients can present with blood glucose (BG) levels of less than 200 mg/dl, which is defined as euglycemic DKA. The possible etiology of euglycemic DKA includes the recent use of insulin, decreased caloric intake, heavy alcohol consumption, chronic liver disease and glycogen storage disorders. DKA in pregnancy has also been reported to present with euglycemia. The recent use of sodium glucose cotransporter 2 (SGLT2) inhibitors has shed light on another possible mechanism of euglycemic DKA. Clinicians may also be misled by the presence of pseudonormoglycemia. Conclusion: Euglycemic DKA thus poses a challenge to physicians, as patients presenting with normal BG levels in ketoacidosis may be overlooked, leading to a delay in appropriate management strategies. In this article, we review all the possible etiologies and the associated pathophysiology of patients presenting with euglycemic DKA. We also discuss the ap Continue reading >>

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Popular Questions

  1. Boykinbaby

    Has anyone done this? I was thinking of giving it a try, cutting my carb intake way back and getting them mostly through green veggies and less dense "starch" veggies and hardly any fruit. My girl is 9 months and still breastfeeding, solids not even enough to consider part of her nutrition yet. Of course I'll up my fat and protein consumption to compensate but advice, tips, ect are greatly appreciated

  2. Renee Lee

    For what purpose would you be consciously entering ketosis for a long period of time? What do you hope to accomplish?

  3. Bethany Lannon

    I'm ebf my 5-month old daughter & I'm also almost to my peak mileage weeks of my marathon training cycle. I have been limiting my starchy veg carbs and fruits, mostly due to wanting to lose fat/gain muscle and also thanks to a carb-phobia I'm still fighting. I'm not sure if its the high running mileage, low carbs (I usually get anywhere from 90-125 carbs per day), or a combination of the two factors but my daughter's weight gain has plummeted. She's still gaining, but lets just say that as of today, she's gained less than 4 lbs since birth, and she's 5 months old. They didn't tell me her weight %ile today, but at her 4-month checkup, it was down to 8.6%. And she only gained 6oz in the last month. So, I'm reluctantly increasing my carbs... I'm going to aim for consistently 150g carbs per day and see if that helps her.
    Obviously with your baby being older, you could get away with cutting carbs *as long as* you start implementing more solids into Baby's diet. My daughter has either butternut squash or avocado 2x per day after nursing, but she's going up to 3x per day as of today (if her weight isn't up more next month at her 6mo visit, they'll talk more about intervening at that point). So, if your baby's primary calories are only coming from you, I'd suggest either holding off on dropping the carbs or implementing more solids to baby's diet first.

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