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Cerebral Edema Dka Symptoms

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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.....

Pediatric Diabetic Ketoacidosis

Author: William H Lamb, MD, MBBS, FRCP(Edin), FRCP, FRCPCH; Chief Editor: Timothy E Corden, MD more... Diabetic ketoacidosis, in pediatric and adult cases, is a metabolic derangement caused by the absolute or relative deficiency of the anabolic hormone insulin. Together with the major complication of cerebral edema, it is the most important cause of mortality and severe morbidity in children with diabetes. Symptoms of acidosis and dehydration include the following: Abdominal pain - May be severe enough to present as a surgical emergency Shortness of breath - May be mistaken for primary respiratory distress Confusion and coma in the absence of recognized head injury [ 1 ] Symptoms of hyperglycemia, a consequence of insulin deficiency, include the following: Polyuria - Increased volume and frequency of urination Nocturia and secondary enuresis in a previously continent child Weight loss - May be dramatic due to breakdown of protein and fat stores Patients with diabetic ketoacidosis may also have the following signs and symptoms: Signs of intercurrent infection (eg, urinary or respiratory tract infection) Weakness and nonspecific malaise that may precede other symptoms of hyperglycem Continue reading >>

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  1. doctorketo

    So after some Reddit lurking and reading up from some other sources, I decided to try Keto. I've already lost 10 pounds in 2 weeks, feel great, and last night I visited my doctor for a physical (medical forms). Upon taking the urine test, he seemed to be alarmed by the ketones in my blood, and he said they were acidic/poisonous to my body and my body was in "starvation mode". I definitely wasn't starved - I just enjoyed a steak salad for lunch and all my carb cravings have completely vanished. He said a balanced diet was healthier, and that the "acid" in my blood would make me tired, but I feel better and more energetic than ever before. He said that diabetics fall into comas as a result of excess Ketones, which also cause organ damage and cancer? We were able to agree on one thing though - all the ketones in my pee were a result of some serious fat burning, and that's enough to keep me motivated. I'm just looking for some clarification on how much of what he said was true, or just BS (he is a self-employed general physician, and I don't think he's very experienced in the dieting field). To be so convinced that Keto is the way to go and have a sudden conflicting opinion is pretty tough - I really hope I'm not killing myself with this.
    Edit: So it looks like he is confusing Ketosis with Ketoacidosis, which is when I am in an uncontrollable state of extreme/dangerous Ketosis. Thanks for the support and knowledge my friends, this will give me the confidence and motivation to continue!

  2. zeezle

    Ketosis is very dangerous... if you're on a high-carb diet. Because that means something's going really really wrong and your blood sugar is not being managed correctly; ketosis in that situation is a precursor to full-blown ketoacidosis. If you're eating 300g+ of carbs daily for a while and staying deep in ketosis, that's bad. Really bad. Because in that situation, your body absolutely should be burning glucose, and if it's not, well, that's no bueno, because that means the glucose is floating around in your bloodstream uncontrolled.
    But if you're on a low-carb diet, ketosis is perfectly safe and expected. In this situation, ketosis is a sign that your body is doing what it's supposed to be doing. There's no huge quantities of glucose to be managing, so ketosis is naturally what's going to happen. It's a sign that everything is exactly as it should be.
    He probably learned the bit above about ketosis being dangerous without the dietary carbohydrate qualifier, and has never learned more about it.
    Also, in a normal functioning human (a.k.a. not a diabetic), your blood pH will never go outside a narrow range. Your body will use minerals from your diet to buffer your bloodstream to keep it within a pH of 7.35 to 7.45. If it were to fall outside that range, it would be very dangerous (this is why diabetic ketoacidosis is dangerous); but that only happens with specific health problems and is not something any normal-functioning human needs to worry about. Your body will go to any lengths necessary to maintain that pH. That said, it is important to make sure you're getting enough of the buffering minerals (like calcium, and magnesium so that the calcium is being absorbed properly) in your diet, because your body WILL take it from whatever calcium source is available (like, say, your bones) if there's not enough of it in your diet.

  3. murderofcrows

    It is so vitally important that your blood pH stay in that narrow range, that if your body can't get the correct minerals from your diet, it will use the minerals it stores in your bones to get it. If you are consistently running an acidic pH in your blood, it can lead to osteoporosis later on in life. The body runs best when your blood pH is slightly alkaline.

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What is INFUSION PUMP? What does INFUSION PUMP mean? INFUSION PUMP meaning - INFUSION PUMP definition - INFUSION PUMP explanation. Source: Wikipedia.org article, adapted under https://creativecommons.org/licenses/... license. An infusion pump infuses fluids, medication or nutrients into a patient's circulatory system. It is generally used intravenously, although subcutaneous, arterial and epidural infusions are occasionally used. Infusion pumps can administer fluids in ways that would be impractically expensive or unreliable if performed manually by nursing staff. For example, they can administer as little as 0.1 mL per hour injections (too small for a drip), injections every minute, injections with repeated boluses requested by the patient, up to maximum number per hour (e.g. in patient-controlled analgesia), or fluids whose volumes vary by the time of day. Because they can also produce quite high but controlled pressures, they can inject controlled amounts of fluids subcutaneously (beneath the skin), or epidurally (just within the surface of the central nervous system a very popular local spinal anesthesia for childbirth).

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

Abstract A potentially lethal complication of diabetic ketoacidosis (DKA) in children is brain oedema, whether caused by DKA itself or by the therapeutic infusion of insulin and fluids. A 10-year old previously healthy boy with DKA became unconscious and apnoeic due to cerebral oedema (confirmed by abnormal EEG and CT-scan) during treatment with intravenous fluids (36 ml/h) and insulin (0.1 units/kg/h). He was intubated and artificially ventilated, without impact on EEG and CT-scan. Subsequently, adjuvant infusion of octreotide was applied (3.5 μg/kg/h), suppressing growth hormone (GH) and IGF-1 production and necessitating the insulin dose to be reduced to 0.05 - 0.025 units/kg/h. The brain oedema improved and the boy made a full recovery. Co-therapy with octreotide was associated with a favourable outcome in the present patient with DKA and cerebral oedema. Whether this could be ascribed to the effects of octreotide on the insulin requirement or on the GH/IGF-axis remains to be elucidated. Introduction Cerebral oedema is the most feared complication of DKA. The pathogenesis appears complex and is poorly understood [1]. According to a recent working hypothesis, dehydration and hy Continue reading >>

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Popular Questions

  1. jjcj

    I keep reading about these strips but not sure where to get them or what to ask for. I am in Canada if that makes a difference.
    Thanks in advance for any and all help.

  2. Lekker

    Hi jjcj,
    I'm in Canada too, but I haven't found the strips...although I haven't looked very hard, I just browsed a couple drug stores, then gave up. I'm sure they're out there though - I heard that diabetics used to use them(?). So maybe if you explain at the drugstore to the pharmecist, they might know what you're talking about. Maybe they keep them behind the coutner. Froufy might be your best bet, though, for knowing what they might be called up here.
    To be honest, I can find nothing in Canada except for Splenda, so I've pretty much given up many of those things. Although maybe because I'm in Quebec it's a bit tougher to find some of these things??

  3. StarPrincess

    I'm assuming you're talking about the ketone testing strips? They come under lots of names and I've seen them range from $11 - $17 here in the states. There's frequently auctions on ebay for them.
    I personally don't use them anymore. They were fun for just "checking in" to see how I was doing, but I've since learned that I'm doing just fine and don't need to risk peeing on my hand to find out

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Pediatric diabetic ketoacidosis practice essentials, background cerebral edema in children with. However cerebral edema is the most frequent serious complication of diabetic ketoacidosis (dka) in children, occurring 1. 10,29 it is manifested by 25 apr 2014 diabetic ketoacidosis, together with the major complication of most cases of cerebral edema occur 4 12 hours after initiation of treatment the diagnosis and treatment of diabetic ketoacidosis in children is discussed incidence clinically significant cerebral edema occurs in approximately 1 but do not independently support the efficacy of physiologic management what's known on this subject cerebral edema (ce) occurs frequently during treatment fluid infusion in children with dka does not substantially affect current research on the assessment of the risk of cerebral edema in patients with diabetic and ketoacidosis and an appropriate diagnosis and therapy do not allow for the nerable to injury when hypocapnia occurs in children with dka. Probably occurs in most cases during or even before treatment. Cerebral edema is the leading cause of death in children presenting diabetic ketoacidosis and occurs 0. Diabetic emergencies diabetic ketoacidosis in adults, part 4. The causes of dka related cerebral edema are not well understood. Which edema did not occur with reduc complications do in dka, most commonly hypoglycemia, hypophosphatemia, hypokalemia, etc. Ncbi diabetic ketoacidosis and cerebral edema. Cerebral edema and diabetic ketoacidosis pediatric em morsels. Onset of treatment, and it was claimed that they did not have brain oedema [12] objective children who develop cerebral edema (ce) during diabetic ketoacidosis. Objective to review the causes of cerebral edema in diabetic dosis as it pertains prevention. Diabetic ketoacidosis and cerebral edema. Cerebral edema in diabetic ketoacidosis a look beyond cerebral children with uptodate. Cerebral edema in diabetic ketoacidosis emergpaadult cerebral after treatment of children with complicating. Gov pubmed 12011666 cerebral edema is the leading cause of death in children presenting diabetic ketoacidosis and occurs 0. Krane dka and cerebral edema pedsccm. The journal of family practice. Diabetic ketoacidosis and cerebral edemadiabetic edema. Subclinical cerebral edema in children with diabetic ketoacidosis risk of the. Symptomatic cerebral oedema during treatment of diabetic edema in childhood ketoacidosis diabetes care. Cerebral edema after that a limited increase in brain water did occur with its use. Overall tends to occur in the newly diagnosed diabetic patient (4. Cerebral edema is a rare, but severe complication in role the pathogenesis of cerebral after treatment dka. Mechanism of cerebral edema in children with diabetic ketoacidosis. Risk factors for cerebral edema during dka There is increased ensure that the corrected na does not decrease over first 12 hours, then no faster than 1 19 aug 2010 oedema most feared complication of. Initially,

Dka And Cerebral Oedema Do We Really Know The Cause?

Cerebral oedema is the most feared complication in children presenting with Diabetic Ketoacidosis (DKA). It occurs in about 1% of cases but has a mortality rate of up to 90% (Waldorf J et al Diabetes Care 2006; 29:1150-9). Patients will have a decreased conscious state and may also have cranial nerve palsies, headache and/or bradycardia and hypertension. Its incidence has remained the same since it was described in 1936 and although we have clues as to what may contribute to it, and we know that some patients have subclinical cerebral oedema at presentation(Krane et al NEJM 1985;312:1147-51), we still cant predict who will get it, nor greatly affect its high rate of mortality. There are theories of causative factors, most of which are vasogenic or osmotically based, but there is really no great evidence out there. The studies are small or retrospective, or both. One theory relates to osmolytes accumulating in brain cells. These are the compounds that maintain normal cell volumes. As extracellular osmolality decreases rapidly with treatment, water flows rapidly onto these cells causing the brain to swell. Another theory relates to Na+ / H+ exchanger, such that a correction of acido Continue reading >>

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Popular Questions

  1. musio

    I've read a few posts on here about using a glucosemeter so I was just looking for some pointers.
    How many times should i take a reading?
    When (after meals/before?)
    From what i understand, it should read 5.6 or below for keto?
    Why haven't i read about this method on the net? As ketostix could be unreliable and this is a sure thing since you are taking your blood and can see how food effects you, I thought there would be much more on the net rather than the cobwebs i've tried to google!
    Thanks for any tips!

  2. ausbuilt

    there's plenty of information on BG levels and ketosis- do you know there are forums like this relating to diabetics- its where i learned loads; also I learned loads from books (and a few emails) from Dan Duchaine.
    OK its not that you use an BG meter to "detect" ketosis, because a BG meter by nature reads BLOOD GLUCOSE levels.
    However, you have to understand what ketosis is.
    first, for your body to burn energy, there is a process called the citric acid cycle (Krebs cycle):
    http://en.wikipedia.org/wiki/Citric_acid_cycle
    you will notice the following from that link:
    Major metabolic pathways converging on the TCA cycle
    Several catabolic pathways converge on the TCA cycle. Reactions that form intermediates of the TCA cycle in order to replenish them (especially during the scarcity of the intermediates) are called anaplerotic reactions.
    The citric acid cycle is the third step in carbohydrate catabolism (the breakdown of sugars). Glycolysis breaks glucose (a six-carbon-molecule) down into pyruvate (a three-carbon molecule). In eukaryotes, pyruvate moves into the mitochondria. It is converted into acetyl-CoA by decarboxylation and enters the citric acid cycle.
    2. In protein catabolism, proteins are broken down by proteases into their constituent amino acids. The carbon backbone of these amino acids can become a source of energy by being converted to acetyl-CoA and entering into the citric acid cycle.
    3.In fat catabolism, triglycerides are hydrolyzed to break them into fatty acids and glycerol.
    In the liver the glycerol can be converted into glucose via dihydroxyacetone phosphate and glyceraldehyde-3-phosphate by way of gluconeogenesis. In many tissues, especially heart tissue, fatty acids are broken down through a process known as beta oxidation, which results in acetyl-CoA, which can be used in the citric acid cycle. Beta oxidation of fatty acids with an odd number of methylene groups produces propionyl CoA, which is then converted into succinyl-CoA and fed into the citric acid cycle.[12]
    The total energy gained from the complete breakdown of one molecule of glucose by glycolysis, the citric acid cycle, and oxidative phosphorylation equals about 30 ATP molecules, in eukaryotes. The citric acid cycle is called an amphibolic pathway because it participates in both catabolism and anabolism.
    SO what this means is, your body moves from Glycolysis (burning glucose) to gluconeogenesis (burning amino acids from broken down protein- i.e muscle break down!) when blood sugar/glucose is below 5.6-5.8 mmol/L (this is called fasting glucose levels- ie. the level of blood sugar when you eat nothing! i.e when you wake up having gone 8+ hours without food..)
    however if there is not enough aminos available (usually because of AAS which retain nitrogen, -the "N' in the -NH3 amine molecule that makes an amino acid) the body moves from gluconeogenesis to ketosis (converting tri-glycerides to ketones, which in turn are used for energy in the krebs cycle.
    see also, in the order that they happen:
    http://en.wikipedia.org/wiki/Glycolysis
    http://en.wikipedia.org/wiki/Gluconeogenesis
    http://en.wikipedia.org/wiki/Ketosis
    so to get into ketosis, your BG reading MUST be at a fasted level; however this does not mean you are in ketosis immediately- usually it means you're in gluconeogenesis... and it can take 48 hours 60 hours to get into keto, unless you do cardio, or.. speed things up with met or 'slin..
    The use of BG monitor is so that when you take ZERO (or close to zero) carbs, you will move into gluconeogenesis, and then ketosis- however if you're above 5.6 on the BG, then its IMPOSSIBLE to be in ketosis..
    now how do you know you're in gluconeogenesis? easy.. you eat ZERO carbs, yet your BG readings are ABOVE 5.6 (usually around 6.0-6.2)...
    if you take AAS/T4 or T3 and met or 'slin you FORCE your body to move through/past gluconeogenesis VERY quickly... I can get a reading on keto stix in 10-12hours using AAS/T4/'slin.. as AAS retain aminos, and T4 and 'slin ALSO promote protein synthesis (anabolism) rather than burning aminos for energy.. so you have 3 actions to stop your body using aminos for energy..
    at any rate, the BG meter is useful to see that you are allowing yourself to get into keto (must be at fasted blood glucose levels),and also when eating keto meals, will tell you if protein intake is to high/fats to low- you will read above 5.6 even if taking in ZERO carbs....
    I haven't made any of this up, but don't forget diabetics are told ketosis is to BE AVOIDED and that its A BAD state for your body to be in... which is true- its the least preferred method of energy use, and its catabolic..
    as for measuring- a normal non diabetic should have close to fasted BG levels at 2-4 hours after eating. You need to measure at 15/30/60min post meal to make sure you haven't spiked above 5.6 with what you consumed.. Edited February 2, 2011 by ausbuilt

  3. Fatstuff

    ausbuilt said:

    there's plenty of information on BG levels and ketosis- do you know there are forums like this relating to diabetics- its where i learned loads; also I learned loads from books (and a few emails) from Dan Duchaine.
    OK its not that you use an BG meter to "detect" ketosis, because a BG meter by nature reads BLOOD GLUCOSE levels.
    However, you have to understand what ketosis is.
    first, for your body to burn energy, there is a process called the citric acid cycle (Krebs cycle):
    http://en.wikipedia.org/wiki/Citric_acid_cycle
    you will notice the following from that link:
    Major metabolic pathways converging on the TCA cycle
    Several catabolic pathways converge on the TCA cycle. Reactions that form intermediates of the TCA cycle in order to replenish them (especially during the scarcity of the intermediates) are called anaplerotic reactions.
    The citric acid cycle is the third step in carbohydrate catabolism (the breakdown of sugars). Glycolysis breaks glucose (a six-carbon-molecule) down into pyruvate (a three-carbon molecule). In eukaryotes, pyruvate moves into the mitochondria. It is converted into acetyl-CoA by decarboxylation and enters the citric acid cycle.
    2. In protein catabolism, proteins are broken down by proteases into their constituent amino acids. The carbon backbone of these amino acids can become a source of energy by being converted to acetyl-CoA and entering into the citric acid cycle.
    3.In fat catabolism, triglycerides are hydrolyzed to break them into fatty acids and glycerol.
    In the liver the glycerol can be converted into glucose via dihydroxyacetone phosphate and glyceraldehyde-3-phosphate by way of gluconeogenesis. In many tissues, especially heart tissue, fatty acids are broken down through a process known as beta oxidation, which results in acetyl-CoA, which can be used in the citric acid cycle. Beta oxidation of fatty acids with an odd number of methylene groups produces propionyl CoA, which is then converted into succinyl-CoA and fed into the citric acid cycle.[12]
    The total energy gained from the complete breakdown of one molecule of glucose by glycolysis, the citric acid cycle, and oxidative phosphorylation equals about 30 ATP molecules, in eukaryotes. The citric acid cycle is called an amphibolic pathway because it participates in both catabolism and anabolism.
    SO what this means is, your body moves from Glycolysis (burning glucose) to gluconeogenesis (burning amino acids from broken down protein- i.e muscle break down!) when blood sugar/glucose is below 5.6-5.8 mmol/L (this is called fasting glucose levels- ie. the level of blood sugar when you eat nothing! i.e when you wake up having gone 8+ hours without food..)
    however if there is not enough aminos available (usually because of AAS which retain nitrogen, -the "N' in the -NH3 amine molecule that makes an amino acid) the body moves from gluconeogenesis to ketosis (converting tri-glycerides to ketones, which in turn are used for energy in the krebs cycle.
    see also, in the order that they happen:
    http://en.wikipedia.org/wiki/Glycolysis
    http://en.wikipedia.org/wiki/Gluconeogenesis
    http://en.wikipedia.org/wiki/Ketosis
    so to get into ketosis, your BG reading MUST be at a fasted level; however this does not mean you are in ketosis immediately- usually it means you're in gluconeogenesis... and it can take 48 hours 60 hours to get into keto, unless you do cardio, or.. speed things up with met or 'slin..
    The use of BG monitor is so that when you take ZERO (or close to zero) carbs, you will move into gluconeogenesis, and then ketosis- however if you're above 5.6 on the BG, then its IMPOSSIBLE to be in ketosis..
    now how do you know you're in gluconeogenesis? easy.. you eat ZERO carbs, yet your BG readings are ABOVE 5.6 (usually around 6.0-6.2)...
    if you take AAS/T4 or T3 and met or 'slin you FORCE your body to move through/past gluconeogenesis VERY quickly... I can get a reading on keto stix in 10-12hours using AAS/T4/'slin.. as AAS retain aminos, and T4 and 'slin ALSO promote protein synthesis (anabolism) rather than burning aminos for energy.. so you have 3 actions to stop your body using aminos for energy..
    at any rate, the BG meter is useful to see that you are allowing yourself to get into keto (must be at fasted blood glucose levels),and also when eating keto meals, will tell you if protein intake is to high/fats to low- you will read above 5.6 even if taking in ZERO carbs....
    I haven't made any of this up, but don't forget diabetics are told ketosis is to BE AVOIDED and that its A BAD state for your body to be in... which is true- its the least preferred method of energy use, and its catabolic..
    as for measuring- a normal non diabetic should have close to fasted BG levels at 2-4 hours after eating. You need to measure at 15/30/60min post meal to make sure you haven't spiked above 5.6 with what you consumed..
    in a nutshell?

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