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 >>
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 >>
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 >>
Thyroid Storm Presenting As Psychosis: Masked By Diabetic Ketoacidosis
While extremely uncommon, diabetic ketoacidosis (DKA) and thyroid storm (TS) are endocrine emergencies that can coexist. We describe a case with a confounding clinical presentation that identifies these two emergencies within the setting of sepsis and influenza. Case A 69-year-old diabetic female was found by the paramedic staff to be disoriented. She demonstrated tachycardia and had a foul-smelling abdominal wound. Laboratory evaluation revealed DKA, leukocytosis, influenza B, and urinary tract infection. After appropriate management in the intensive care unit, the DKA resolved the following morning. However, the patient developed a fever, and her psychosis became more pronounced. Extensive analysis was performed but did not explain her mental status. The patient was found to have thyroid stimulating hormone of 0.06 mIU/mL, free T4 (thyroxine) of 2.38 ng/dL, and total T3 (triiodothyronine) of 72 ng/dL. Based on the Burch and Wartofsky criteria (score of 65), TS was diagnosed. Based on more recent diagnostic criteria suggested by Akamizu et al., the patient met criteria for TS grade 1. Within several hours of initiating treatment, the patient's mental state and tachycardia improved, and her psychosis resolved by the third day. This case highlights the importance of recognizing the clinical diagnosis of TS, as the magnitude of thyroid hormone derangements may not correlate with clinical severity. While rare, DKA and TS can simultaneously occur and are associated with increased morbidity and mortality if not promptly recognized and treated. Continue reading >>
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 >>
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 >>
Management Of Diabetic Ketoacidosis In Adults
Diabetic ketoacidosis is a potentially life-threatening complication of diabetes, making it a medical emergency. Nurses need to know how to identify and manage it and how to maintain electrolyte balance Continue reading >>
Diabetic Ketoacidosis (dka)
Diabetic Ketoacidosis (DKA) Admission criteria: -Always admit diabetic ketoacidosis to the hospital. In fact, these patients need to be admitted to the ICU for constant monitoring and IV insulin. Pearls: -DKA can be precitated by an infection or other body stresses. -Symptoms include polyuria, polydipsia, nausea, vomiting, fatigue, abdominal pain, tachycardia seconday to dehydration, signs of an underlying infection, kussmauls respirations secondary to metabolic acidosis, changes in mental status (from lethargy to coma). (Source: AAFP, March 2013, Diabetic Ketoacidosis: Evaluation and Treatment). -Differentiate this from hyperglycemic hyperosmolar state (HHS) - HHS does no or trace keytones, while DKA is always positive for keytones. HHS has a variable anion gap. Blood pH in HHS is > 7.3, and in DKA pH is < 7.3. Serum osmolality is always > 320 in HHS. Serum HCO3 is always > 18 in HHS, and less than 18 in DKA (Source: AAFP, March 2013, Diabetic Ketoacidosis: Evaluation and Treatment). (Source: AAFP, March 2013, Diabetic Ketoacidosis: Evaluation and Treatment) -The differential diagnosis includes HHS, lactic acidosis, high anion gap metabolic acidosis, alcoholic ketoacidosis, pancreatitis, starvation ketosis. -The primary keytone in DKA is beta-hydroxybutyrate. -The sodium can appear low, but this is because of hyperglycemia, where fluid follows the glucose because of osmolarity, and dilutes the sodium, so calculate corrected sodium. -Because a DKA patient is often dehydrated, hemoglobin and WBC can be elevated due to dehydration; therefore, to assess the possibility of infection, look for bandemia. -Calculate anion gap, this is the (Na - (Cl + HCO3)). Normal anion gap is 7-13 mEq/L. -Normal serum osmolality is 285-295 mOsm/kg. -Cerebral edema is the most severe complica Continue reading >>
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 >>
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 >>
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
EM Week, Day 1 Diabetic Ketoacidosis (DKA) is a life threatening condition in which insufficient insulin levels result in metabolism of fatty acids & production of ketone bodies causing severe metabolic acidosis. Classically seen as the first presentation of T1DM, it can also present after a period of missed insulin doses in either type. Typically symptoms include neurological manifestations such as lethargy, focal signs (SUCH AS), or obtundation; abdominal pain; and tachypnea. The classic “fruity breath” and Kussmaul (deep) respirations may also be present. Diagnosis is made rapidly on blood gas showing acidosis with increased anion gap, low bicarbonate, (usually) moderate hyperglycemia, and increased ketones in serum / urine. Treatment is resuscitation with IV fluids (NS) and IV insulin. Electrolytes (Na, K, PO4, glucose) monitoring/correction is important. Acidosis causes efflux of K+ (in response to transcellular H+ shift) and a relative hyperkalemia which, when corrected, can overshoot and result in hypokalemia. Sodium bicarb infusion is only indicated if pH<6.9. Monitor response to treatment with serial VBGs looking at bicarb (resolution of metabolic acidosis) and anion gap (resolution of ketoacidemia), not BGL. DKA is considered resolved when anion gap is <12 (normal), plasma osmolarity <315, and patient is alert & able to eat. Interestingly, a new T2DM drug class called SGLT-2 inhibitors (“-gliflozins,” inhibit renal resorption of glucose), are associated w euglycemic ketoacidosis typically seen after periods of fasting (i.e. pre-op). While rare, this is important to remember because the use of these drugs is increasing due results of the EMPA-REG trial showing 38% relative risk reduction in cardiovascular mortality in T2 diabetics with established CVD. 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 >>
- Relative effectiveness of insulin pump treatment over multiple daily injections and structured education during flexible intensive insulin treatment for type 1 diabetes: cluster randomised trial (REPOSE)
- Diabetic Ketoacidosis
- Diabetic Ketoacidosis Increases Risk of Acute Renal Failure in Pediatric Patients with Type 1 Diabetes
Diabetic Ketoacidosis
Diabetic Ketoacidosis (DKA) is a metabolic emergency occurring in Type 1 diabetes. It is characterised by the following: Acidosis: Blood pH below 7.3 or plasma bicarbonate below 18mmol/litre Ketonaemia: Blood ketones (beta-hydroxybutyrate) above 3mmol/litre Hyperglycaemia: Blood glucose levels are generally high (above 11mmol/litre), although children with known Type 1 diabetes can less commonly develop DKA with normal blood glucose levels DKA can be life threatening. The three complications which account for the majority of deaths in these children are cerebral oedema, hypokalaemia and aspiration pneumonia. An understanding of the principles discussed in the ‘Approach to the Seriously Unwell Child’ article and an awareness of the British Society of Paediatric Endocrinology and Diabetes (BSPED) guideline for DKA management (1) will help you manage these children appropriately. 31,500 children and young people under the age of 19 in the UK have diabetes. The vast majority of them (over 95%), have Type 1 Diabetes Mellitus (T1DM.) The peak age for diagnosis is between 9 and 14 years (2). In established T1DM, the risk of DKA is 1–10% per patient per year (3). Reported mortality rates from DKA in children in the UK are around 0.3%, the majority of which are attributable to cerebral oedema, which has a mortality rate of 25 % (4). T1DM can be seen as ‘starvation in the midst of plenty,’ where blood glucose levels are raised as it cannot be used for metabolism or stored due to an absolute deficiency of insulin. This leads to a rise in counter-regulatory hormones including glucagon, cortisol, catecholamines and growth hormone. The increase in these gluconeogenic hormones not only raises the blood glucose concentration further, but also leads to accelerated break down o Continue reading >>
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 >>
