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When Is Dka Considered Resolved

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is an acute, life-threatening complication of diabetes mellitus. The incidence and prevalence of diabetes are rising; as of 2005, an estimated 7% of the U.S. population had diabetes. In patients age 60 or older, the prevalence is estimated to be 20.9%.1 DKA occurs predominately in patients with type 1 (insulin-dependent) diabetes mellitus, but unprovoked DKA can occur in newly diagnosed type 2 (non–insulin-dependent) diabetes mellitus, especially in blacks and Hispanics.2 Between 1993 and 2003, the yearly rate of ED visits for DKA per 10,000 U.S. population with diabetes was 64, with a trend toward an increased rate of visits among the black population compared with the white population.3 Europe has a comparable incidence. A better understanding of pathophysiology and an aggressive, uniform approach to diagnosis and management have reduced mortality to <5% of reported episodes in experienced centers.4 However, mortality is higher in the elderly due to underlying renal disease or coexisting infection and in the presence of coma or hypotension. DKA is a response to cellular starvation brought on by relative insulin deficiency and counterregulatory or catabolic hormone excess (Figure 220-1). Insulin is the only anabolic hormone produced by the endocrine pancreas and is responsible for the metabolism and storage of carbohydrates, fat, and protein. Counterregulatory hormones include glucagon, catecholamines, cortisol, and growth hormone. Complete or relative absence of insulin and the excess counterregulatory hormones result in hyperglycemia (due to excess production and underutilization of glucose), osmotic diuresis, prerenal azotemia, worsening hyperglycemia, ketone formation, and a wide-anion gap metabolic acidosis.4 Insulin deficiency. Patho Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Initial Evaluation Initial evaluation of patients with DKA includes diagnosis and treatment of precipitating factors (Table 14–18). The most common precipitating factor is infection, followed by noncompliance with insulin therapy.3 While insulin pump therapy has been implicated as a risk factor for DKA in the past, most recent studies show that with proper education and practice using the pump, the frequency of DKA is the same for patients on pump and injection therapy.19 Common causes by frequency Other causes Selected drugs that may contribute to diabetic ketoacidosis Infection, particularly pneumonia, urinary tract infection, and sepsis4 Inadequate insulin treatment or noncompliance4 New-onset diabetes4 Cardiovascular disease, particularly myocardial infarction5 Acanthosis nigricans6 Acromegaly7 Arterial thrombosis, including mesenteric and iliac5 Cerebrovascular accident5 Hemochromatosis8 Hyperthyroidism9 Pancreatitis10 Pregnancy11 Atypical antipsychotic agents12 Corticosteroids13 FK50614 Glucagon15 Interferon16 Sympathomimetic agents including albuterol (Ventolin), dopamine (Intropin), dobutamine (Dobutrex), terbutaline (Bricanyl),17 and ritodrine (Yutopar)18 DIFFERENTIAL DIAGNOSIS Three key features of diabetic acidosis are hyperglycemia, ketosis, and acidosis. The conditions that cause these metabolic abnormalities overlap. The primary differential diagnosis for hyperglycemia is hyperosmolar hyperglycemic state (Table 23,20), which is discussed in the Stoner article21 on page 1723 of this issue. Common problems that produce ketosis include alcoholism and starvation. Metabolic states in which acidosis is predominant include lactic acidosis and ingestion of drugs such as salicylates and methanol. Abdominal pain may be a symptom of ketoacidosis or part of the inci Continue reading >>

The Management Of Diabetic Ketoacidosis In Adults

The Management Of Diabetic Ketoacidosis In Adults

Action 1: Commence 0.9% sodium chloride solution (use large bore cannula) via infusion pump. See Box 2 for rate of fluid replacement Action 2: Commence a fixed rate intravenous insulin infusion (IVII). (0.1unit/kg/hr based on estimate of weight) 50 units human soluble insulin (Actrapid® or Humulin S®) made up to 50ml with 0.9% sodium chloride solution. If patient normally takes long acting insulin analogue (Lantus®, Levemir®) continue at usual dose and time Action 3: Assess patient o Respiratory rate; temperature; blood pressure; pulse; oxygen saturation o Glasgow Coma Scale o Full clinical examination Action 4: Further investigations • Capillary and laboratory glucose • Venous BG • U & E • FBC • Blood cultures • ECG • CXR • MSU Action 5: Establish monitoring regimen • Hourly capillary blood glucose • Hourly capillary ketone measurement if available • Venous bicarbonate and potassium at 60 minutes, 2 hours and 2 hourly thereafter • 4 hourly plasma electrolytes • Continuous cardiac monitoring if required • Continuous pulse oximetry if required Action 6: Consider and precipitating causes and treat appropriately BOX 1: Immediate management: time 0 to 60 minutes (T=0 at time intravenous fluids are commenced) If intravenous access cannot be obtained request critical care support immediately Systolic BP (SBP) below 90mmHg Likely to be due to low circulating volume, but consider other causes such as heart failure, sepsis, etc. • Give 500ml of 0.9% sodium chloride solution over 10-15 minutes. If SBP remains below 90mmHg repeat whilst requesting senior input. Most patients require between 500 to 1000ml given rapidly. • Consider involving the ITU/critical care team. • Continue reading >>

Treatment Of Diabetic Ketoacidosis With Subcutaneous Insulin Aspart

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 >>

Diagnosis And Treatment Of Diabetic Ketoacidosis

Diagnosis And Treatment Of Diabetic Ketoacidosis

85 Abstract Diabetic ketoacidosis (DKA) is the most frequent hyperglycaemic acute diabetic complication. Furthermore it carries a significant risk of death, which can be prevented by early and effective management. All physicians, irrespective of the discipline they are working in and whether in primary, secondary or tertiary care institutions, should be able to recognise DKA early and initiate management immediately. 86 Introduction Diabetic ketoacidosis (DKA) is a common complication of diabetes with an annual occurrence rate of 46 to 50 per 10 000 diabetic patients. The severity of this acute diabetic complication can be appreciated from the high death-to-case ratio of 5 to 10%.1 In Africa the mortality of DKA is unacceptably high with a reported death rate of 26 to 29% in studies from Kenya, Tanzania and Ghana.2 It is a complication of both type 1 and type 2 diabetes mellitus, although more commonly seen in type 1 diabetic patients. Of known diabetic patients presenting with DKA about one-quarter will be patients with type 2 diabetes. In patients presenting with a DKA as first manifestation of diabetes about 15% will be type 2.3 This correlates well with data from South Africa suggesting that one- quarter of patients with DKA will be type 2 with adequate C-peptide levels and the absence of anti-GAD antibodies.4 This review will focus on the principles of diagnosis, monitoring and treatment of DKA, with special mention of new developments and controversial issues. Clinical features DKA evolves over hours to days in both type 1 and type 2 diabetic patients, but the symptoms of poor control of blood glucose are usually present for several days before the onset or presentation of ketoacidosis.5 The clinical features of DKA are non-specific and patients may present with Continue reading >>

Management Of Diabetic Ketoacidosis In Children And Adolescents

Management Of Diabetic Ketoacidosis In Children And Adolescents

Objectives After completing this article, readers should be able to: Describe the typical presentation of diabetic ketoacidosis in children. Discuss the treatment of diabetic ketoacidosis. Explain the potential complications of diabetic ketoacidosis that can occur during treatment. Introduction Diabetic ketoacidosis (DKA) represents a profound insulin-deficient state characterized by hyperglycemia (>200 mg/dL [11.1 mmol/L]) and acidosis (serum pH <7.3, bicarbonate <15 mEq/L [15 mmol/L]), along with evidence of an accumulation of ketoacids in the blood (measurable serum or urine ketones, increased anion gap). Dehydration, electrolyte loss, and hyperosmolarity contribute to the presentation and potential complications. DKA is the most common cause of death in children who have type 1 diabetes. Therefore, the best treatment of DKA is prevention through early recognition and diagnosis of diabetes in a child who has polydipsia and polyuria and through careful attention to the treatment of children who have known diabetes, particularly during illnesses. Presentation Patients who have DKA generally present with nausea and vomiting. In individuals who have no previous diagnosis of diabetes mellitus, a preceding history of polyuria, polydipsia, and weight loss usually can be elicited. With significant ketosis, patients may have a fruity breath. As the DKA becomes more severe, patients develop lethargy due to the acidosis and hyperosmolarity; in severe DKA, they may present with coma. Acidosis and ketosis cause an ileus that can lead to abdominal pain severe enough to raise concern for an acutely inflamed abdomen, and the elevation of the stress hormones epinephrine and cortisol in DKA can lead to an elevation in the white blood cell count, suggesting infection. Thus, leukocytosi Continue reading >>

Childhood Ketoacidosis

Childhood Ketoacidosis

Patient professional reference Professional Reference articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use. You may find one of our health articles more useful. Diabetic ketoacidosis (DKA) is the leading cause of mortality in childhood diabetes.[1]The primary cause of DKA is absolute or relative insulin deficiency: Absolute - eg, previously undiagnosed type 1 diabetes mellitus or a patient with known type 1 diabetes who does not take their insulin. Relative - stress causes a rise in counter-regulatory hormones with relative insulin deficiency. DKA can be fatal The usual causes of death are: Cerebral oedema - associated with 25% mortality (see 'Cerebral odedema', below). Hypokalaemia - which is preventable with good monitoring. Aspiration pneumonia - thus, use of a nasogastric tube in the semi-conscious or unconscious is advised. Deficiency of insulin. Rise in counter-regulatory hormones, including glucagon, cortisol, growth hormone, and catecholamines. Thus, inappropriate gluconeogenesis and liver glycogenolysis occur compounding the hyperglycaemia, which causes hyperosmolarity and ensuing polyuria, dehydration and loss of electrolytes. Accelerated catabolism from lipolysis of adipose tissue leads to increased free fatty acid circulation, which on hepatic oxidation produces the ketone bodies (acetoacetic acid and beta-hydroxybutyric acid) that cause the metabolic acidosis. A vicious circle is usually set up as vomiting usually occurs compounding the stress and dehydration; the cycle can only be broken by providing insulin and fluids; otherwise, severe acidosis occurs and can be fatal. Biochemical criteria The biochemical criteria required for a diagnosis of DKA to be made are Continue reading >>

Diabetic Ketoacidosis Producing Extreme Hyperkalemia In A Patient With Type 1 Diabetes On Hemodialysis

Diabetic Ketoacidosis Producing Extreme Hyperkalemia In A Patient With Type 1 Diabetes On Hemodialysis

Hodaka Yamada1, Shunsuke Funazaki1, Masafumi Kakei1, Kazuo Hara1 and San-e Ishikawa2[1] Division of Endocrinology and Metabolism, Jichi Medical University Saitama Medical Center, Saitama, Japan [2] Division of Endocrinology and Metabolism, International University of Health and Welfare Hospital, Nasushiobara, Japan Summary Diabetic ketoacidosis (DKA) is a critical complication of type 1 diabetes associated with water and electrolyte disorders. Here, we report a case of DKA with extreme hyperkalemia (9.0 mEq/L) in a patient with type 1 diabetes on hemodialysis. He had a left frontal cerebral infarction resulting in inability to manage his continuous subcutaneous insulin infusion pump. Electrocardiography showed typical changes of hyperkalemia, including absent P waves, prolonged QRS interval and tented T waves. There was no evidence of total body water deficit. After starting insulin and rapid hemodialysis, the serum potassium level was normalized. Although DKA may present with hypokalemia, rapid hemodialysis may be necessary to resolve severe hyperkalemia in a patient with renal failure. Patients with type 1 diabetes on hemodialysis may develop ketoacidosis because of discontinuation of insulin treatment. Patients on hemodialysis who develop ketoacidosis may have hyperkalemia because of anuria. Absolute insulin deficit alters potassium distribution between the intracellular and extracellular space, and anuria abolishes urinary excretion of potassium. Rapid hemodialysis along with intensive insulin therapy can improve hyperkalemia, while fluid infusions may worsen heart failure in patients with ketoacidosis who routinely require hemodialysis. Background Diabetic ketoacidosis (DKA) is a very common endocrinology emergency. It is usually associated with severe circulatory Continue reading >>

Case Report Severe Allergic Reaction To Human Insulin In The Patient With Diabetic Ketoacidosis

Case Report Severe Allergic Reaction To Human Insulin In The Patient With Diabetic Ketoacidosis

1. Introduction Diabetic ketoacidosis (DKA) is a potentially fatal crisis of diabetes mellitus (DM). In the treatment of DKA, fluid resuscitation, insulin therapy, and electrolyte replacement are important. Rarely, insulin allergies can be developed in the patient treated with insulin. The most common symptoms of insulin allergies are localized and limited. Life-threatening allergic reactions are rarely reported. Insulin allergies can be managed safely and successfully by desensitization treatment.1,2 We present treatment of a patient with DKA who developed an insulin allergy. In this case report, we aimed to discuss DKA treatment options in patient with insulin allergies. 2. Case report A 45-year-old male was brought to our emergency department with chest pain and hyperglycemia. He had a history of type 2 DM and had been using an oral antidiabetic drug for two years, but he had been stopped using for a month. HIs past medical history did not show any drug allergies. His vitals were measured: 1.) blood pressure of 166/98 mmHg; 2.) pulse 100/min; 3.) respiration number 24/min; 4.) O2 saturation 98%; and 5.) temperature 36.0 °C. His electrocardiograms (ECG's) were normal. His blood glucose level was 405 mg/dL, urinary ketones 15 mmol/L, pH was 6.8, HCO3 4.7 mmol/L, and lactate 3.6 mmol/L. Regular insulin (0.1unit/kg IV bolus) was initiated in addition to 2000 mL of intravenous saline, and a 0.1 unit/kg/hour infusion was started. He developed a generalized skin rash, hoarseness, and uvular edema at the 30th minute of treatment, which then expanded to the soft palate. The vital findings were normal except for the presence of tachycardia. At that moment his vitals were measured: 1.) blood pressure 126/75 mmHg; 2.) pulse 104/min; 3.) respiration number 24/min; 4.) O2 saturat Continue reading >>

66: Diabetic Ketoacidosis (dka) And Hyperosmolar Hyperglycemic State (hhs)

66: Diabetic Ketoacidosis (dka) And Hyperosmolar Hyperglycemic State (hhs)

In this episode I’ll discuss diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS). Subscribe on iTunes, Android, or Stitcher Definition Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are the most serious acute complications of diabetes. These diabetic crises cause thousands of deaths annually in the US. DKA and HHS differ clinically according to the presence of ketoacidosis and the degree of hyperglycemia. In DKA metabolic acidosis is often the major finding. The serum glucose is below 800 mg/dL and usually in the 350-500 mg/dL range. DKA usually evolves rapidly. In HHS, there is little or no ketoacidosis and the serum glucose concentration frequently exceeds 1000 mg/dL. HHS usually evolves over a period of several days. Overlap between DKA and HHS occurs in more than one-third of patients. Pathogenesis Insulin deficiency/resistance and glucagon excess are responsible for the development of DKA and HHS. The deficiency in insulin (either absolute or relative deficiency) is more severe in DKA compared with HHS. In HHS the residual insulin secretion and its systemic activity minimizes the development of ketoacidosis but is not adequate to control hyperglycemia. In patients with absolute or relative insulin deficiency, DKA and HHS are usually precipitated by a stressor such as infection or discontinuation of / inadequate insulin therapy. Treatment The treatment of DKA and HHS involves the correction of fluid and electrolyte abnormalities, followed by the administration of insulin. Specific treatment protocols include: ADA guidelines, Joslin protocol, and Yale New Haven. The order of treatment is essential. A patient in DKA or HHS is already volume-depleted. Insulin forces glucose as well as potassium and water into cells. Therefor Continue reading >>

Diabetes & Dka Study Set

Diabetes & Dka Study Set

Sort What are some EARLY SYMPTOMS of hypoglycaemia? Shaking, trembling or weakness Sweating Paleness Hunger Light headedness Headache Dizziness Pins and needles around mouth Mood change What are some LATER SIGNS of hypoglycaemia? Lack of concentration/ behaviour change Confusion Slurred speech Not able to treat own hypo Not able to drink or swallow Not able to follow instructions Loss of consciousness Fitting/seizures What is Diabetic Ketoacidosis (DKA)? A triad of: 1. Hyperglycaemia 2. Ketosis 3. Metabolic acidosis that develops in the setting of insulin deficiency. - body begins to burn fat for energy instead leading to accumulation of dangerous chemicals in the blood called ketones (ketonaemia) and in the urine (ketonuria). What are some SYMPTOMS of DKA? Extreme Hyperglycaemia with moderate to heavy Ketones in the urine with: - Rapid breathing - Flushed cheeks, hot, dry skin - Abdominal pain - Sweet acetone smell on the breath - Emesis (vomiting) - Polydipsia (feeling thirsty) - Polyuria (urinating a lot) - blurred vision Why do pts with DKA get polyuria, polydipsia and blurred vision? BGLs are so high that osmotic diuresis occurs - Water follows the glucose concentration passively, leading to abnormally high urine output. - Kidneys are forced to work overtime to filter and absorb the excess sugar - If your kidneys can't keep up, the excess sugar is excreted into your urine, dragging along fluids from your tissues. This triggers more frequent urination, which may leave you dehydrated. As you drink more fluids (polydipsia) to quench your thirst, you'll urinate even more. - vision is affected due to fluid being dragged from eye tissues. How is DKA assessed to determine severity? Blood ketones Blood glucose Venous bicarbonate Venous (or aterial) pH Potassium (if <3.5mmo Continue reading >>

Diabetic Ketoacidosis Treatment & Management

Diabetic Ketoacidosis Treatment & Management

Approach Considerations Managing diabetic ketoacidosis (DKA) in an intensive care unit during the first 24-48 hours always is advisable. When treating patients with DKA, the following points must be considered and closely monitored: It is essential to maintain extreme vigilance for any concomitant process, such as infection, cerebrovascular accident, myocardial infarction, sepsis, or deep venous thrombosis. It is important to pay close attention to the correction of fluid and electrolyte loss during the first hour of treatment. This always should be followed by gradual correction of hyperglycemia and acidosis. Correction of fluid loss makes the clinical picture clearer and may be sufficient to correct acidosis. The presence of even mild signs of dehydration indicates that at least 3 L of fluid has already been lost. Patients usually are not discharged from the hospital unless they have been able to switch back to their daily insulin regimen without a recurrence of ketosis. When the condition is stable, pH exceeds 7.3, and bicarbonate is greater than 18 mEq/L, the patient is allowed to eat a meal preceded by a subcutaneous (SC) dose of regular insulin. Insulin infusion can be discontinued 30 minutes later. If the patient is still nauseated and cannot eat, dextrose infusion should be continued and regular or ultra–short-acting insulin should be administered SC every 4 hours, according to blood glucose level, while trying to maintain blood glucose values at 100-180 mg/dL. The 2011 JBDS guideline recommends the intravenous infusion of insulin at a weight-based fixed rate until ketosis has subsided. Should blood glucose fall below 14 mmol/L (250 mg/dL), 10% glucose should be added to allow for the continuation of fixed-rate insulin infusion. [19, 20] In established patient Continue reading >>

What Is A Dka Disease?

What Is A Dka Disease?

Diabetic ketoacidosis (DKA) is a life-threatening condition that develops when cells in the body are unable to get the sugar (glucose) they need for energy because there is not enough insulin. When the sugar cannot get into the cells, it stays in the blood. The kidneys filter some of the sugar from the blood and remove it from the body through urine. Because the cells cannot receive sugar for energy, the body begins to break down fat and muscle for energy. When this happens, ketones, or fatty acids, are produced and enter the bloodstream, causing the chemical imbalance (metabolic acidosis) called diabetic ketoacidosis. What causes DKA? Ketoacidosis can be caused by not getting enough insulin, having a severe infection or other illness, becoming severely dehydrated, or some combination of these things. It can occur in people who have little or no insulin in their bodies (mostly people with type 1 diabetes but it can happen with type 2 diabetes, especially children) when their blood sugar levels are high. What are the symptoms? Your blood sugar may be quite high before you notice symptoms, which include: Flushed, hot, dry skin. Blurred vision. Feeling thirsty and urinating a lot. Drowsiness or difficulty waking up. Young children may lack interest in their normal activities. Rapid, deep breathing. A strong, fruity breath odor. Loss of appetite, belly pain, and vomiting. Confusion. Continue reading >>

When Does A Startup Stop Being A Startup And Become A Normal Company?

When Does A Startup Stop Being A Startup And Become A Normal Company?

All companies start off as start-ups. Once a company reaches a point where it seems very likely it will still be around in four years, then it is no longer a start-up. And once a company goes public (at least in the U.S.), it is no longer a start-up. Once you are no longer a start-up, you can never, ever become a start-up again. (just like you can never actually be a teenager again even though you can still act like one) By this definition (writing in December 2016), Uber is NOT a start-up but Lyft still is a start-up. The corner grocery that has been around for 20 years is not a start-up but the new hip coffee shop next door is. Snapchat started 2016 as a start-up … now it is no longer a start-up. My subjective values: No longer a start-up: AirBNB, Palantir, Xiaomi, Didi Chuxing, Snapchat, Uber, SpaceX Still a start-up (but might might not be in 2017): Dropbox, Pintrest, Lyft, Flipkart, Stripe, Spotify, Magic Leap, Cloudera, Social Finance, Docusign, Oscar Health, Github, Instacart, MongoDB, Mulesoft, Flatiron Health, Appnexus, Docker, Cloudflare, Hootsuite, Gusto, Glassdoor, and many others. 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 >>

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