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Diabetic Ketoacidosis

Diabetic Ketoacidosis

Also known as: DKA Severe diabetic ketoacidosis is a medical emergency and requires prompt treatment to correct dehydration, electrolyte disturbances and acidosis. It is a complication of insulin dependent Diabetes Mellitus. DKA is the result of marked insulin deficiency, and ketonaemia and ketoacidosis occur approximately 15 days after insulin concentrations are suppressed to fasting levels. Marked insulin suppression occurs on average 4 days after fasting glucose levels reach 30mmol/L. Many cats with DKA have other intercurrent conditions which may precipitate the condition including: infection, pancreatitis or renal insufficiency. Pathophysiology Insulin deficiency leads to increased breakdown of fat that releases fatty acids into the circulation. Free fatty acids are oxidised in the liver to ketones that are used by many tissues as an energy source instead of glucose. This occurs when intracellular levels of glucose are insufficient for energy metabolism as a result of severe insulin deficiency. In the liver, instead of being converted to triglycerides, free fatty acids are oxidised to acetoacetate, which is converted to hydroxybutyrate or acetone. Ketones are acids that cause central nervous system depression and act in the chemoreceptor trigger zone to cause nausea, vomiting and anorexia. They also accelerate osmotic water loss in the urine. Dehydration results from inadequate fluid intake in the face of accelerated water loss due to glucosuria and ketonuria. Dehydration and subsequent reduced tissue perfusion compounds the acidosis through lactic acid production. There is whole body loss of electrolytes including sodium, potassium, magnesium and phosphate and there is also intracellular redistribution of electrolytes following insulin therapy which may compound p Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

4 Evaluation 5 Management Defining features include hyperglycemia (glucose > 250mg/dl), acidosis (pH < 7.3), and ketonemia/ketonuria Leads to osmotic diuresis and depletion of electrolytes including sodium, magnesium, calcium and phosphorous. Further dehydration impairs glomerular filtration rate (GFR) and contributes to acute renal failure Due to lipolysis / accumulation of of ketoacids (represented by increased anion gap) Compensatory respiratory alkalosis (i.e. tachypnea and hyperpnea - Kussmaul breathing) Breakdown of adipose creates first acetoacetate leading to conversion to beta-hydroxybutyrate Causes activation of RAAS in addition to the osmotic diuresis Cation loss (in exchange for chloride) worsens metabolic acidosis May be the initial presenting of an unrecognized T1DM patient Presenting signs/symptoms include altered mental status, tachypnea, abdominal pain, hypotension, decreased urine output. Perform a thorough neurologic exam (cerebral edema increases mortality significantly, especially in children) Assess for possible inciting cause (especially for ongoing infection; see Differential Diagnosis section) Ill appearance. Acetone breath. Drowsiness with decreased reflexes Tachypnea (Kussmaul's breathing) Signs of dehydration with dry mouth and dry mucosa. Perform a thorough neurologic exam as cerebral edema increases mortality significantly, especially in children There may be signs from underlying cause (eg pneumonia) Differential Diagnosis Insulin or oral hypoglycemic medication non-compliance Infection Intra-abdominal infections Steroid use Drug abuse Pregnancy Diabetic ketoacidosis (DKA) Diagnosis is made based on the presence of acidosis and ketonemia in the setting of diabetes. Bicarb may be normal due to compensatory and contraction alcoholosis so the Continue reading >>

Ketoacidosis In A Patient With Type 2 Diabetes – Flatbush Diabetes

Ketoacidosis In A Patient With Type 2 Diabetes – Flatbush Diabetes

There is increasing recognition of a group of patients with type 2 diabetes who can present with ketoacidosis. Most reports have been of patients of African descent; however, the condition has been reported in other groups. This is a case of a Caucasian patient who has had three presentations with ketoacidosis and whose diabetes is not usually insulin-dependent. A patient, aged 48 years, presented with diabetic ketoacidosis (DKA) in a semi-comatose condition. She had a 3-day history of vomiting and loss of appetite. In the previous weeks she had undergone radiotherapy for metastatic squamous cell carcinoma (skin primary). The patient had two similar episodes of DKA, one 20 months and another 3 months earlier. Two of the patient’s brothers had type 2 diabetes. The patient was not abusing alcohol and did not have a history of pancreatitis. Three years prior to this admission the patient had been diagnosed elsewhere with type 2 diabetes, for which she had been on metformin and a small dose of insulin glargine. Two months after stopping her insulin glargine she developed her first episode of DKA while visiting our town. DKA, was diagnosed on the basis of arterial pH 7.03, blood glucose level 25.9 mmol/L, bicarbonate level of 5 mmol/L and positive urinary ketones. It was felt that infected skin lesions may have precipitated the DKA. Eleven days later, she was discharged on metformin 250 mg twice daily and a falling dose of insulin glargine (26 units a day). She was then lost to follow-up in our centre, but apparently soon after did not require insulin and maintained adequate gylcaemic control for 18 months until just prior to her next admission solely on metformin 1 g twice daily. The next admission for DKA occurred while living in a city. She was discharged on insulin but Continue reading >>

Ketone Bodies

Ketone Bodies

Ketone bodies Acetone Acetoacetic acid (R)-beta-Hydroxybutyric acid Ketone bodies are three water-soluble molecules (acetoacetate, beta-hydroxybutyrate, and their spontaneous breakdown product, acetone) that are produced by the liver from fatty acids[1] during periods of low food intake (fasting), carbohydrate restrictive diets, starvation, prolonged intense exercise,[2], alcoholism or in untreated (or inadequately treated) type 1 diabetes mellitus. These ketone bodies are readily picked up by the extra-hepatic tissues, and converted into acetyl-CoA which then enters the citric acid cycle and is oxidized in the mitochondria for energy.[3] In the brain, ketone bodies are also used to make acetyl-CoA into long-chain fatty acids. Ketone bodies are produced by the liver under the circumstances listed above (i.e. fasting, starving, low carbohydrate diets, prolonged exercise and untreated type 1 diabetes mellitus) as a result of intense gluconeogenesis, which is the production of glucose from non-carbohydrate sources (not including fatty acids).[1] They are therefore always released into the blood by the liver together with newly produced glucose, after the liver glycogen stores have been depleted (these glycogen stores are depleted after only 24 hours of fasting)[1]. When two acetyl-CoA molecules lose their -CoAs, (or Co-enzyme A groups) they can form a (covalent) dimer called acetoacetate. Beta-hydroxybutyrate is a reduced form of acetoacetate, in which the ketone group is converted into an alcohol (or hydroxyl) group (see illustration on the right). Both are 4-carbon molecules, that can readily be converted back into acetyl-CoA by most tissues of the body, with the notable exception of the liver. Acetone is the decarboxylated form of acetoacetate which cannot be converted Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Diabetic Ketoacidosis Definition Diabetic ketoacidosis is a dangerous complication of diabetes mellitus in which the chemical balance of the body becomes far too acidic. Description Diabetic ketoacidosis (DKA) always results from a severe insulin deficiency. Insulin is the hormone secreted by the body to lower the blood sugar levels when they become too high. Diabetes mellitus is the disease resulting from the inability of the body to produce or respond properly to insulin, required by the body to convert glucose to energy. In childhood diabetes, DKA complications represent the leading cause of death, mostly due to the accumulation of abnormally large amounts of fluid in the brain (cerebral edema). DKA combines three major features: hyperglycemia, meaning excessively high blood sugar kevels; hyperketonemia, meaning an overproduction of ketones by the body; and acidosis, meaning that the blood has become too acidic. Insulin deficiency is responsible for all three conditions: the body glucose goes largely unused since most cells are unable to transport glucose into the cell without the presence of insulin; this condition makes the body use stored fat as an alternative source instead of the unavailable glucose for energy, a process that produces acidic ketones, which build up because they require insulin to be broken down. The presence of excess ketones in the bloodstream in turn causes the blood to become more acidic than the body tissues, which creates a toxic condition. Causes and symptoms DKA is most commonly seen in individuals with type I diabetes, under 19 years of age and is usually caused by the interruption of their insulin treatment or by acute infection or trauma. A small number of people with type II diabetes also experience ketoacidosis, but this is rare give Continue reading >>

Diabetic Coma

Diabetic Coma

Diabetic coma is a reversible form of coma found in people with diabetes mellitus. It is a medical emergency.[1] 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[edit] Severe hypoglycemia[edit] 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 >>

Diabetic Ketoacidosis - Symptoms

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 >>

Ketosis

Ketosis

Not to be confused with Ketoacidosis. Ketosis is a metabolic state in which some of the body's energy supply comes from ketone bodies in the blood, in contrast to a state of glycolysis in which blood glucose provides energy. Ketosis is a result of metabolizing fat to provide energy. Ketosis is a nutritional process characterised by serum concentrations of ketone bodies over 0.5 mM, with low and stable levels of insulin and blood glucose.[1][2] It is almost always generalized with hyperketonemia, that is, an elevated level of ketone bodies in the blood throughout the body. Ketone bodies are formed by ketogenesis when liver glycogen stores are depleted (or from metabolising medium-chain triglycerides[3]). The main ketone bodies used for energy are acetoacetate and β-hydroxybutyrate,[4] and the levels of ketone bodies are regulated mainly by insulin and glucagon.[5] Most cells in the body can use both glucose and ketone bodies for fuel, and during ketosis, free fatty acids and glucose synthesis (gluconeogenesis) fuel the remainder. Longer-term ketosis may result from fasting or staying on a low-carbohydrate diet (ketogenic diet), and deliberately induced ketosis serves as a medical intervention for various conditions, such as intractable epilepsy, and the various types of diabetes.[6] In glycolysis, higher levels of insulin promote storage of body fat and block release of fat from adipose tissues, while in ketosis, fat reserves are readily released and consumed.[5][7] For this reason, ketosis is sometimes referred to as the body's "fat burning" mode.[8] Ketosis and ketoacidosis are similar, but ketoacidosis is an acute life-threatening state requiring prompt medical intervention while ketosis can be physiological. However, there are situations (such as treatment-resistant Continue reading >>

Diabetic Ketoacidosis (dka)

Diabetic Ketoacidosis (dka)

take bloods for FBE, U&E, blood gas, ketones, glucose, osmolality, troponin (if adult), blood cultures stat IV 0.9% saline 15-20 mL/kg in first hour (eg. for adults 1-1.5L stat) if initial K+ < 4mM, give iv KCl to correct K= before starting insulin if pH < 6.9, consider iv sodium bicarbonate (see below) consider empirical iv antibiotics AVOID arterial line unless severe DKA with pH < 6.9 consider prophylactic anticoagulation, esp. if elderly with hyperosmolar state aims of Rx: re-hydrate with 0.9% NS at 4-14 mL/kg/hr ongoing insulin infusion as per protocol 5% dextrose infusion once glucose falls below 15mMol/L at rate of 1L over 8hrs regular blood glucose, blood gas, K+ assessments (eg. hrly initially then 4hrly) monitor for complications: Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is a medical emergency that can happen in people with diabetes mellitus. DKA happens mostly in people with Type 1 diabetes, although it may happen in some people that have Type 2 diabetes. DKA happens when a person does not have enough insulin in their body. All of the cells in the body need glucose (sugar) to survive, because the body needs sugar to make energy. Insulin breaks down glucose into a form that the body can use for energy. Without insulin, sugar stays in the blood and cannot get into the cells. This causes high blood sugar levels and makes it impossible for the cells to use glucose to make energy. DKA can be caused by not having enough insulin, eating too many carbohydrates, and sometimes physical or mental stress. DKA can also be a sign that a person has diabetes that has not been discovered, or is not being controlled well. DKA is diagnosed through blood and urine testing. These tests will show high blood sugar, which does not happen with other forms of ketoacidosis. DKA was first discovered around 1886. Before insulin therapy was first used in the 1920s, DKA almost always caused death. The "3 polys" of DKA: Polydipsia (feeling very thirsty; this is caused by dehydration) Polyphagia (feeling very hungry; the brain realizes the body's cells are not getting enough sugar and triggers hunger, because normally eating would give the cells the sugar they need) Polyuria (urinating a lot; this is the body's way of trying to get rid of the extra glucose in the bloodstream) A "fruity" smell on the breath (acetone breath, caused by the body trying to blow off the acids and waste products created by DKA) Abdominal pain As DKA gets worse, it can cause these symptoms:[2] Confusion, which becomes worse and worse (because the brain is not getti Continue reading >>

Ketoacidosis

Ketoacidosis

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 β-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.[1] 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.[2] Ketosis may also give off an odor, 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. Cause[edit] Three common causes of ketoacidosis are alcohol, starvation, and diabetes, resulting in alcoholic ketoacidosis, starvation ketoacidosis, and diabetic ketoacidosis respectively.[3] In diabetic ketoacidosis, a high concentration of ketone bodies is usually accomp Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is a serious complication of diabetes mellitus and should be regarded as a medical emergency. DKA is defined as a severe metabolic acidosis of blood (pH <7.35) which occurs secondary to sustained fatty acid (ketones) release from fat stores in response to energy demands experienced by feline diabetic patients. Classically, DKA is characterised by metabolic acidosis, ketosis and ketonuria. It can sometimes be confused with feline hyperosmolar hyperglycaemic state. The two main ketones are acetoacetate and β-hydroxybutyrate, which are produced by the liver and serve as an energy source for tissue in times of low insulin levels. (prolonged fasting, starvation, diabetes mellitus) or insulin resistance[1]. Clinical signs Clinical signs include sudden collapse, dehydration, weakness, depression, vomiting, and an increased respiratory rate. DKA can occur at any age and there is no breed or gender predisposition with this disease. It appears commonly in obese cats or cats with a history of sudden weight gain. Concurrent disease predispose cats, especially diabetic ones to developing DKA. Concurrent illnesses include chronic renal disease, hepatic lipidosis, acute pancreatitis, bacterial or viral infections and neoplasia[2]. Hyperglycaemia and hypoinsulinaemia contribute significantly to a shift of potassium to the extracellular fluid. However, with rehydration, potassium ions are lost from the extracellular fluid and hypokalemia develops rapidly. Insulin therapy may worsen hypokalemia because insulin shifts potassium into cells. The most important clinical significance of hypokalemia in DKA is profound muscle weakness, which may result in ventroflexion of the neck and, in extreme cases, respiratory paralysis. In one study of cats with DKA, most cats Continue reading >>

Starvation-induced True Diabetic Euglycemic Ketoacidosis In Severe Depression

Starvation-induced True Diabetic Euglycemic Ketoacidosis In Severe Depression

Go to: A 34-year-old man with a 19-year history of type 1 diabetes presented as an emergency with a 4-day history of nausea, vomiting, and flu-like symptoms. He was on a basal bolus insulin regime comprising 8 units of bolus insulin lispro injected at mealtimes and 12 units of basal isophane insulin at bedtime, but did not monitor capillary blood glucose levels. He did however empirically increase his insulin doses during times of illness and had increased his isophane insulin to 15 units during the 3 days prior to presentation. He had only one prior hospital admission, which occurred 6 years previously and was due to an episode of DKA precipitated by gastroenteritis. He was single, unemployed, did not drink alcohol, had no previous psychiatric history, no family history of diabetes or other medical conditions, and lived in a hostel. He had a record of poor clinic attendances and a history of long-term cannabis use. He denied any salicylate consumption, but admitted to some weight loss; however, he was unable to quantify this. His body mass index (BMI) was 19 kg/m2, and he looked unkempt. Physical examination revealed a temperature of 36.4°C (97.5°F), heart rate of 106 beats per minute, supine blood pressure of 131/85 mmHg, and sitting blood pressure of 122/80 mmHg. He had a respiratory rate of 30 breaths per minute, and his oxygen saturation using a pulsoximeter was 99% on room air. He appeared clinically dehydrated with dry oral mucosa, but cardiovascular, respiratory, abdominal, and neurological examinations were otherwise normal. Diabetic ketoacidosis (DKA) was suspected; metabolic acidosis was confirmed with a pH of 7.3, bicarbonate concentration of 10 mEq/l, and an elevated anion gap of 29 mEq/l [sodium = 134 mEq/l, potassium = 5.7 mEq/l, chloride = 101 mEq/l, b Continue reading >>

Alcoholic Ketoacidosis.

Alcoholic Ketoacidosis.

AKA is an acute metabolic disorder that occurs in ethanol abusers who have usually had a recent binge and who, because of gastritis or another intercurrent illness, stop eating and drinking and often vomit repeatedly. This causes dehydration and ketoacidosis which, unlike in diabetics, is usually associated with little or no hyperglycemia or glucosuria. Despite the ketoacidosis, blood pH findings are variable, depending on the severity of coexisting metabolic alkalosis (owing to vomiting) and respiratory alkalosis (owing to pain or delirium tremens). The metabolic disorders respond rapidly and gratifyingly to parenteral rehydration and administration of glucose, potassium salts, and thiamine. Insulin is usually not necessary, except in patients known or suspected to have diabetes. Because some patients have serious coexisting acute illnesses (which may even have precipitated the acute metabolic disorder), assiduous search for those and the appropriate treatment are essential. The prognosis for the acute metabolic disorder per se is excellent, that for coexisting illness depends on the illness, and that for the ethanol abuse is still often problematic.[1] References Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Use Continue reading >>

Euglycemic Dka: It’s Not A Myth

Euglycemic Dka: It’s Not A Myth

Background: Diabetic ketoacidosis (DKA) is traditionally defined as a triad of hyperglycemia (>250mg/dL), anion gap acidosis, and increased plasma ketones. There is another entity that providers must be aware of known as euglycemic DKA (euDKA), which is essentially DKA without the hyperglycemia (Serum glucose <200 mg/dL). Euglycemic DKA is a rare entity that mostly occurs in patients with type 1 diabetes, but can possibly occur in type 2 diabetes as well. The exact mechanism of euDKA is not entirely known, but has been associated with partial treatment of diabetes, carbohydrate food restriction, alcohol intake, and inhibition of gluconeogenesis. euDKA, can also be associated with sodium-glucose cotransporter 2 (SGLT-2) inhibitor medications. These medications first came onto the market in 2013 and are FDA approved for the treatment of type 2 diabetes, however many physicians use them off-label for type I diabetes due to their ability to improve average glucose levels, reduce glycemic variability without increasing hypoglycemia, and finally promote weight loss. Does euDKA Exist even in Patients not Using SGLT-2 Inhibitors? The short answer is YES. Munro JF et al [5] reviewed a case series of 37 episodes of euDKA in a publication from 1973. Although, dated and not robust evidence some take home messages can be derived: All but one episode was in insulin dependent diabetics Vomiting was the most frequent symptom of euDKA in 32% of patients Management in most cases consisted of: Intravenous fluids and electrolyte replacement. No deaths occurred in this case series What are the Names of the SGLT-2 Inhibitors? Ipragliflozin (Suglat) – Approved in Japan Dapagliflozin (Farxiga) – 1st SGLT2 Inhibitor Approved; Approved in US Luseogliflozin (Lusefi) – Approved in Japan Tofo Continue reading >>

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