How Is Ketoacidosis Treated

What Is The Longest A Diabetic Can Go Without An Injection?

Type one diabetes at the most two to three days, by that time they would be severely ketotic, risking a sometimes fatal diabetes hyperglycemic ketoacidotic coma. For type 2 diabetes mostly that can be for months, even years, like we see in those war torn areas. My erstwhile partner, when I met him already a senior physician, told me that the experience during WW II in The Netherlands, those mostly type 2 diabetics who couldn’t get insulin didn’t die from not having insulin (which at the end was air-dropped by the British into German occupied territories), in fact did quite well with their blood sugars, unfortunately for a very sad reason: the Dutch famine of 1944–45 - Wikipedia costing about 18,000 people their lives. Of course not having their diabetes well controlled would cause them to develop a lot more complications so would shorten their lifespan appreciably. Continue reading >>

Diabetes: What Is Ketoacidosis And How Can Be Avoided & Treated?

Good question! According to Wikipedia: Diabetic ketoacidosis is a potentially life-threatening complication in patients with diabetes mellitus. In order to define ketoacidosis a little better, let's go back to the source: diabetes. Someone who is diabetic is unable to produce insulin, a hormone necessary for the transfer of sugar from the bloodstream to the cells, which in turn produce energy. If this progression is disrupted, through lack of insulin for example, the body has to try to compensate by creating energy elsewhere. And so the body starts to burn fat and muscle to meet its energy needs. Unfortunately, this chemical reaction produces molecules known as ketone bodies. In small quantities, these are fine, and it is in fact normal to have traces of them in your blood (approximately 1mg/dl). However, if the quantity of ketones surpasses this threshold by too much, it starts to affect the pH of your blood (which becomes progressively more acidic). Even the slightest drop in pH can have dangerous effects: as the quantity of the ketones in your blood increases, and the blood pH diminishes, your kidneys start having problems. Eventually, if the ketoacidosis is left untreated, your kidneys can fail and you can die from dehydration, tachycardia and hypotension. A number of other symptoms can appear in extreme cases. Fortunately for us, the quantity of ketones has to be consequential, and it usually takes a while before individuals start manifesting symptoms. In my case, my diabetes went undiagnosed for a month and a half before it was discovered, and even then my ketone levels were relatively normal. If you're a diabetic, ketoacidosis can be easily avoided by controlling your blood sugar levels and maintaining a healthy lifestyle. Some doctors, preferring to stay on the Continue reading >>

What Kind Of Diseases Result In Death Within 2 Weeks Of Diagnosis?

How to cure serious Diseases by a simple Meditation So now let's start the procedure. Before starting the meditation procedure, first check that you have very deep belief within yourself that you can go to any heights to cure your diseases and even if it will not be cured even then you have strongest belief that you will try every possible effort to cure it. Then, if you have that strong belief then start the procedure. Sit in a cross legged position with eyes closed. And try to do what I tell you here, if you cannot do it perfectly then at least keep your belief upon doing all this. Don't think anything, forget the world and everything in it, also forget that you have any illness and need to recover from it, forget that you are doing meditation for something. Then try to look into God's eyes, but forget any of the worldly Gods. Just look into the eyes of the God which comes to your mind naturally without any thinking. And then you will see slowly in 1-2 weeks your illness passes away. I hope this will do it and that too without any heavy and cumbersome medical procedure. Continue reading >>

Treatment And Complications Of Diabetic Ketoacidosis In Children And Adolescents

INTRODUCTION Diabetic ketoacidosis (DKA) is the leading cause of morbidity and mortality in children with type 1 diabetes mellitus (T1DM), with a case fatality rate ranging from 0.15 percent to 0.31 percent [1-3]. DKA also can occur in children with type 2 DM (T2DM); this presentation is most common among youth of African-American descent [4-8]. (See "Classification of diabetes mellitus and genetic diabetic syndromes".) The management of DKA in children will be reviewed here (table 1). There is limited experience in the management and outcomes of DKA in children with T2DM, although the same principles should apply. The clinical manifestations and diagnosis of DKA in children and the pathogenesis of DKA are discussed elsewhere. (See "Clinical features and diagnosis of diabetic ketoacidosis in children and adolescents" and "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Epidemiology and pathogenesis".) DEFINITION Diabetic ketoacidosis – A consensus statement from the International Society for Pediatric and Adolescent Diabetes (ISPAD) in 2014 defined the following biochemical criteria for the diagnosis of diabetic ketoacidosis (DKA) [9]: Hyperglycemia – Blood glucose of >200 mg/dL (11 mmol/L) AND Metabolic acidosis – Venous pH <7.3 or a plasma bicarbonate <15 mEq/L (15 mmol/L) AND Continue reading >>

Diabetes With Ketone Bodies In Dogs

Studies show that female dogs (particularly non-spayed) are more prone to DKA, as are older canines. Diabetic ketoacidosis is best classified through the presence of ketones that exist in the liver, which are directly correlated to the lack of insulin being produced in the body. This is a very serious complication, requiring immediate veterinary intervention. Although a number of dogs can be affected mildly, the majority are very ill. Some dogs will not recover despite treatment, and concurrent disease has been documented in 70% of canines diagnosed with DKA. Diabetes with ketone bodies is also described in veterinary terms as diabetic ketoacidosis or DKA. It is a severe complication of diabetes mellitus. Excess ketone bodies result in acidosis and electrolyte abnormalities, which can lead to a crisis situation for your dog. If left in an untreated state, this condition can and will be fatal. Some dogs who are suffering from diabetic ketoacidosis may present as systemically well. Others will show severe illness. Symptoms may be seen as listed below: Change in appetite (either increase or decrease) Increased thirst Frequent urination Vomiting Abdominal pain Mental dullness Coughing Fatigue or weakness Weight loss Sometimes sweet smelling breath is evident Slow, deep respiration. There may also be other symptoms present that accompany diseases that can trigger DKA, such as hypothyroidism or Cushing’s disease. While some dogs may live fairly normal lives with this condition before it is diagnosed, most canines who become sick will do so within a week of the start of the illness. There are four influences that can bring on DKA: Fasting Insulin deficiency as a result of unknown and untreated diabetes, or insulin deficiency due to an underlying disease that in turn exacerba Continue reading >>

What Are Some Ways To Treat Early Signs Of Ketoacidosis?

Other than take your insulin, your body triggers natural treatments. In ketoacidosis, you are lacking insulin or your insulin is not effective in converting glucose into energy. You generally have too much actual glucose in your system but your body can’t use it without good insulin. Therefore, your body starts breaking down fat to turn into energy. A byproduct of breaking down fat into energy is ketones. Because of the high sugar, your body will want to dilute it and you’ll be thirsty. As you drink fluids, it will help flush the ketones out through the kidneys, making you pee a lot. In addition, your blood will be in an acidic state. One method of trying to correct this acidic state is to quickly create a respiratory alkalosis state by getting rid of carbon dioxide. You start breathing deeply and quickly; we call this kussmaul breathing. These are the body’s attempt of regulating what it deems as a problem. Generally this cascade of problems is due to an infection or something else wrong in the body and can come on quickly. You really need to get in and see a doctor quickly to get it taken care of properly. Continue reading >>

Management Of Adult Diabetic Ketoacidosis

Go to: Abstract Diabetic ketoacidosis (DKA) is a rare yet potentially fatal hyperglycemic crisis that can occur in patients with both type 1 and 2 diabetes mellitus. Due to its increasing incidence and economic impact related to the treatment and associated morbidity, effective management and prevention is key. Elements of management include making the appropriate diagnosis using current laboratory tools and clinical criteria and coordinating fluid resuscitation, insulin therapy, and electrolyte replacement through feedback obtained from timely patient monitoring and knowledge of resolution criteria. In addition, awareness of special populations such as patients with renal disease presenting with DKA is important. During the DKA therapy, complications may arise and appropriate strategies to prevent these complications are required. DKA prevention strategies including patient and provider education are important. This review aims to provide a brief overview of DKA from its pathophysiology to clinical presentation with in depth focus on up-to-date therapeutic management. Keywords: DKA treatment, insulin, prevention, ESKD Go to: Introduction In 2009, there were 140,000 hospitalizations for diabetic ketoacidosis (DKA) with an average length of stay of 3.4 days.1 The direct and indirect annual cost of DKA hospitalizations is 2.4 billion US dollars. Omission of insulin is the most common precipitant of DKA.2,3 Infections, acute medical illnesses involving the cardiovascular system (myocardial infarction, stroke) and gastrointestinal tract (bleeding, pancreatitis), diseases of the endocrine axis (acromegaly, Cushing’s syndrome), and stress of recent surgical procedures can contribute to the development of DKA by causing dehydration, increase in insulin counter-regulatory hor Continue reading >>

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 (dka)

Diabetic ketoacidosis is an acute metabolic complication of diabetes characterized by hyperglycemia, hyperketonemia, and metabolic acidosis. Hyperglycemia causes an osmotic diuresis with significant fluid and electrolyte loss. DKA occurs mostly in type 1 diabetes mellitus (DM). It causes nausea, vomiting, and abdominal pain and can progress to cerebral edema, coma, and death. DKA is diagnosed by detection of hyperketonemia and anion gap metabolic acidosis in the presence of hyperglycemia. Treatment involves volume expansion, insulin replacement, and prevention of hypokalemia. Diabetic ketoacidosis (DKA) is most common among patients with type 1 diabetes mellitus and develops when insulin levels are insufficient to meet the body’s basic metabolic requirements. DKA is the first manifestation of type 1 DM in a minority of patients. Insulin deficiency can be absolute (eg, during lapses in the administration of exogenous insulin) or relative (eg, when usual insulin doses do not meet metabolic needs during physiologic stress). Common physiologic stresses that can trigger DKA include Some drugs implicated in causing DKA include DKA is less common in type 2 diabetes mellitus, but it may occur in situations of unusual physiologic stress. Ketosis-prone type 2 diabetes is a variant of type 2 diabetes, which is sometimes seen in obese individuals, often of African (including African-American or Afro-Caribbean) origin. People with ketosis-prone diabetes (also referred to as Flatbush diabetes) can have significant impairment of beta cell function with hyperglycemia, and are therefore more likely to develop DKA in the setting of significant hyperglycemia. SGLT-2 inhibitors have been implicated in causing DKA in both type 1 and type 2 DM. Continue reading >>

Diabetic Ketoacidosis

Treatment Approach The main goals of treatment are: Restoration of volume deficits Resolution of hyperglycemia and ketosis/acidosis Correction of electrolyte abnormalities (potassium level should be >3.3 mEq/L before initiation of insulin therapy; use of insulin in a patient with hypokalemia may lead to respiratory paralysis, cardiac arrhythmias, and death) Treatment of the precipitating events and prevention of complications. It must be emphasized that successful treatment requires frequent monitoring of clinical and laboratory parameters to achieve resolution criteria. A treatment protocol and a flow sheet for recording the treatment stages and laboratory data should be maintained. [1] [38] [39] [40] Initial and supportive treatment The majority of patients present to the emergency department, where treatment should be initiated. There are several important steps that should be followed in early management: Fluid therapy should be started immediately after initial laboratory evaluations. Infusion of isotonic solution of 0.9% sodium chloride at a rate of 1 to 1.5 L/hour should be used for the first hour of fluid therapy. Indications for admission to the intensive care unit (ICU) are hemodynamic instability or cardiogenic shock, altered mental status, respiratory insufficiency, severe acidosis, and hyperosmolar state with coma. The diagnosis of hemodynamic instability should made by observing for hypotension and clinical signs of poor tissue perfusion, including oliguria, cyanosis, cool extremities, and altered mental state. After admission to ICU, central venous and arterial lines are required, with continuous percutaneous oximetry. Oxygenation and airway protection are critical. Intubation and mechanical ventilation are commonly required, with constant monitoring of r Continue reading >>

Is Type 1 Diabetes More Dangerous Than Type 2?

Type 1 diabetes results from a rheumatoid-like autoimmune reaction in which one’s own body attacks and destroys the beta cells of the pancreas. These are the cells that normally produce insulin. Type 1 is a disease in which the patient in a relatively short time has no insulin production. All patients with type 1 diabetes can also develop a serious metabolic disorder called ketoacidosis when their blood sugars are high and there is not enough insulin in their body. Ketoacidosis can be fatal unless treated as an emergency with hydration and insulin. Type 2 diabetes rates are growing dramatically in the United States and Western Europe. Type 2 is the result of the muscles and other tissues of the body developing a resistance to insulin produced by the beta cells of the pancreas. The pancreas first tries to overcome this resistance to insulin by making more insulin. The blood sugar goes up as a patient’s body is no longer able to make enough insulin. Most patients with type 2 diabetes mellitus are overweight or obese. For most, but not all, maintenance of a normal weight and a good diet will prevent development of type 2 diabetes. Most type 2 diabetes is diagnosed after age 40. For this reason, many have referred to type 2 as adult-onset diabetes mellitus. This latter name has lost favor as the obesity epidemic has caused a number of people to be diagnosed with type 2 as early as 10 or 11. Type 2 can often be treated with diet modification and can improve significantly with weight loss and exercise. Some patients will be effectively treated with medications such as metformin that increase peripheral sensitivity of organs to insulin. Still more severe disease will require oral medications that encourage the pancreas to make more insulin such as glyburide or glipizide So Continue reading >>

Diabetic Ketoacidosis (dka)

Diabetic ketoacidosis is an acute metabolic complication of diabetes characterized by hyperglycemia, hyperketonemia, and metabolic acidosis. Hyperglycemia causes an osmotic diuresis with significant fluid and electrolyte loss. DKA occurs mostly in type 1 diabetes mellitus (DM). It causes nausea, vomiting, and abdominal pain and can progress to cerebral edema, coma, and death. DKA is diagnosed by detection of hyperketonemia and anion gap metabolic acidosis in the presence of hyperglycemia. Treatment involves volume expansion, insulin replacement, and prevention of hypokalemia. Diabetic ketoacidosis (DKA) is most common among patients with type 1 diabetes mellitus and develops when insulin levels are insufficient to meet the body’s basic metabolic requirements. DKA is the first manifestation of type 1 DM in a minority of patients. Insulin deficiency can be absolute (eg, during lapses in the administration of exogenous insulin) or relative (eg, when usual insulin doses do not meet metabolic needs during physiologic stress). Common physiologic stresses that can trigger DKA include Some drugs implicated in causing DKA include DKA is less common in type 2 diabetes mellitus, but it may occur in situations of unusual physiologic stress. Ketosis-prone type 2 diabetes is a variant of type 2 diabetes, which is sometimes seen in obese individuals, often of African (including African-American or Afro-Caribbean) origin. People with ketosis-prone diabetes (also referred to as Flatbush diabetes) can have significant impairment of beta cell function with hyperglycemia, and are therefore more likely to develop DKA in the setting of significant hyperglycemia. SGLT-2 inhibitors have been implicated in causing DKA in both type 1 and type 2 DM. Continue reading >>

Treatment Of Diabetic Ketoacidosis With Subcutaneous Insulin Aspart

Abstract OBJECTIVE—In this prospective, randomized, open trial, we compared the efficacy and safety of aspart insulin given subcutaneously at different time intervals to a standard low-dose intravenous (IV) infusion protocol of regular insulin in patients with uncomplicated diabetic ketoacidosis (DKA). RESEARCH DESIGN AND METHODS—A total of 45 consecutive patients admitted with DKA were randomly assigned to receive subcutaneous (SC) aspart insulin every hour (SC-1h, n = 15) or every 2 h (SC-2h, n = 15) or to receive IV infusion of regular insulin (n = 15). Response to medical therapy was evaluated by assessing the duration of treatment until resolution of hyperglycemia and ketoacidosis. Additional end points included total length of hospitalization, amount of insulin administration until resolution of hyperglycemia and ketoacidosis, and number of hypoglycemic events. RESULTS—Admission biochemical parameters in patients treated with SC-1h (glucose: 44 ± 21 mmol/l [means ± SD], bicarbonate: 7.1 ± 3 mmol/l, pH: 7.14 ± 0.09) were similar to those treated with SC-2h (glucose: 42 ± 21 mmol/l, bicarbonate: 7.6 ± 4 mmol/l, pH: 7.15 ± 0.12) and IV regular insulin (glucose: 40 ± 13 mmol/l, bicarbonate 7.1 ± 4 mmol/l, pH: 7.11 ± 0.17). There were no statistical differences in the mean duration of treatment until correction of hyperglycemia (6.9 ± 4, 6.1 ± 4, and 7.1 ± 5 h) or until resolution of ketoacidosis (10 ± 3, 10.7 ± 3, and 11 ± 3 h) among patients treated with SC-1h and SC-2h or with IV insulin, respectively (NS). There was no mortality and no differences in the length of hospital stay, total amount of insulin administration until resolution of hyperglycemia or ketoacidosis, or the number of hypoglycemic events among treatment groups. CONCLUSIONS—Ou Continue reading >>

Low-dose Insulin In The Treatment Of Diabetic Ketoacidosis

Severe diabetic ketoacidosis remains a lethal condition. Many deaths occur during therapy and are avoidable. Treatment includes rehydration, administration of insulin and potassium, and clinical care. For many years very large doses of insulin were used. Recently, it has been suggested that such large doses are unnecessary and lead to undue hypokalemia, hypoglycemia, and osmotic disequilibria. Many studies are now available that show that low doses of insulin given as continuous intravenous infusions (4 to 10 units/hr) or as hourly intramuscular injections (20 units initially, then 5 units/ hr) are as effective as large doses in treating severe ketoacidosis. The new regimens are simple to use, predictable, and safe. Potassium shifts are less than with large insulin doses and insulin resistance has been shown to be a relatively minor problem. The new regimens are particularly suitable for use in nonspecialist centers. (Arch Intern Med 137:1367-1376, 1977) Continue reading >>

Fluid Management In Diabetic Ketoacidosis

Young people with insulin dependent diabetes mellitus are three times more likely to die in childhood than the general population.1 Despite advances in management over the past 20 years, the incidence of mortality associated with diabetic ketoacidosis (DKA) remains unchanged. Cerebral oedema is the predominant cause of this mortality; young children are particularly at risk, with an incidence of 0.7–1% of episodes of DKA.2,3 The mortality appears to be greatest among patients at first presentation,1,3,4 if there has been a long history of symptoms prior to admission,3 and during the first 24 hours of treatment.4 In a recently published retrospective multicentre analysis of children with DKA, low pco2 levels and high serum sodium concentration at presentation were identified as particular risk factors for the development of cerebral oedema, together with bicarbonate therapy.5 However, in the accompanying editorial, Dunger and Edge point out that this may simply be revealing an association between severe DKA and dehydration and the risk of cerebral oedema.6 The pathogenesis of cerebral oedema remains poorly understood but there may be many contributing factors.7 The aim of management of DKA is to restore metabolic homoeostasis while minimising the risks of complications including hypoglycaemia, hypokalaemia, cardiac failure, and in children the development of cerebral oedema. How best to achieve this remains contentious, with particular controversy centred on optimal fluid management. The most appropriate volume, type, and rate of fluid to be given have all been the subject of debate. A survey in 1994 of UK paediatricians found a threefold variation in the amount of fluid recommended within the first 12 hours.8 Since then national guidelines have been developed by the B Continue reading >>