Diabetic Ketoacidiosis
Objectives Introduction and awareness of the pathophysiology of Diabetic Ketoacidosis Clinical recognition,establishing a diagnosis and assessment of co-morbidities Clinical Management of DKA and recognition of complications Introduction: State of absolute or relative insulin deficiency aggravated by ensuing hyperglycemia, dehydration, and acidosis-producing derangements in intermediary metabolism. Characterized by Hyperglycemia over 300 mg/dL Low bicarbonate (<15 mEq/L) Acidosis (pH <7.30) Ketonemia and ketonuria. Path physiology Insulin deficiency Increased counter-regulatory hormones (ie, glucagon, cortisol, growth hormone, epinephrine). Enhanced hepatic gluconeogenesis, glycogenolysis, and lipolysis Osmolality Measured as 2(Na+) (mEq/L) + glucose (mg/dL)/18 + BUN(mg/dL)/2.8. Patients with DKA who are in a coma typically have osmolalities >330 mOsm/kg H20. If the osmolality is less than this in a comatose patient, search for another cause of obtundation. Repeat labs are critical Potassium needs to be checked every 1-2 hours during initial treatment. Glucose and other electrolytes should be checked every 2 hours or so during initial aggressive volume, glucose, and electrolyte management. If the initial phosphorous was low, it should be monitored every 4 hours during therapy. Other complications CVT MI Acute gastric dilatation Erosive gastritis Late hypoglycemia Respiratory distress Infection Continue reading >>
Cerebral Edema And Diabetic Ketoacidosis
Cerebral edema is the most feared emergent complication of pediatric diabetic ketoacidosis. Fortunately, it is relatively rare, but the rarity can lead to some confusion when it comes to its management. We recently discussed the use of mannitol and hypertonic saline for pediatric traumatic brain injury, but when should we consider these medications for the patient presenting with DKA? Cerebral Edema is a relatively rare. Incidence <1% of patients with DKA. Overall tends to occur in the newly diagnosed diabetic patient (4.3% vs 1.2%). While rare, it is a devastating complication. 1990 study showed case fatality rate was 64%. Those treated BEFORE respiratory failure had lower rate of mortality (30%). Lesson = treat early! The exact mechanism is not known… and may be varied between individual patients. Signs and Symptoms develop in: 66% within the first 7 hours of treatment (these tend to be younger). 33% within 10-24 hours of treatment. The diagnosis is clinical! ~40% of initial brain imaging of kids with cerebral edema are NORMAL! This is the area that often leads to finger pointing… most often those fingers being pointed toward the Emergency Physician who was initially caring for the kid. Much of the literature focused on interventions, but: Administration of Bicarb Sodium Bicarb was shown to be associated with Cerebral Edema in one study… Unfortunately, this study did not adjust for illness severity. Type of IV Fluids Generally, there is an absence of evidence that associates volume, tonicity, or rate change in serum glucose with Cerebral Edema development. There are cases presenting with cerebral edema prior to any therapies. Risk Factors that seem to stay consistent: Kids < 5 years of age More likely to have delayed diagnosis More severely ill at presentation S Continue reading >>
Canadian Diabetes Association Clinical Practice Guidelines Hyperglycemic Emergencies In Adults
guidelines.diabetes.ca | 1-800-BANTING (226-8464) | diabetes.ca Copyright © 2013 Canadian Diabetes Association 1 Clinical Practice Guidelines CPG Tool Kit Professional Publications Diabetes Educator Study Resources & Educator Resources Food and Nutrition Tools CDA-CSEM Annual Conference Key Points Suspect DKA or HHS in an ill patient with hyperglycemia (usually) – medical emergency DKA = ketoacidosis is prominent HHS = ECFV contraction + hyperosmolarity Rx = FLUIDS, POTASSIUM, INSULIN (DKA) Treat precipitating cause Prevention is critical 2013 guidelines.diabetes.ca | 1-800-BANTING (226-8464) | diabetes.ca Copyright © 2013 Canadian Diabetes Association 2 Clinical Practice Guidelines CPG Tool Kit Professional Publications Diabetes Educator Study Resources & Educator Resources Food and Nutrition Tools CDA-CSEM Annual Conference Hyperglycemic Emergencies DKA = Diabetic Ketoacidosis HHS = Hyperosmolar Hyperglycemic State Common features: Insulin deficiency ïƒ hyperglycemia ïƒ urinary loss of water and electrolytes ïƒ Volume depletion + electrolyte deficiency + hyperosmolarity Insulin deficiency (absolute) + glucagon ïƒ Ketoacidosis (in DKA) guidelines.diabetes.ca | 1-800-BANTING (226-8464) | diabetes.ca Copyright © 2013 Canadian Diabetes Association 3 Clinical Practice Guidelines CPG Tool Kit Professional Publications Diabetes Educator Study Resources & Educator Resources Food and Nutrition Tools CDA-CSEM Annual Conference DKA Ketoacidosis ECFV contraction Milder hyperosmolarity Normal to high glucose May haveLOC Beware hypokalemia Must use insulin Absolute insulin deficiency + glucagon HHS Minimal acid-base problem ECFV contraction Hyperosmolarity Marked hyperglycemia Marked LOC Beware hypokalemia May need insulin Relative insulin Continue reading >>
Diabetic Ketoacidosis
Professor of Pediatric Endocrinology University of Khartoum, Sudan Introduction DKA is a serious acute complications of Diabetes Mellitus. It carries significant risk of death and/or morbidity especially with delayed treatment. The prognosis of DKA is worse in the extremes of age, with a mortality rates of 5-10%. With the new advances of therapy, DKA mortality decreases to > 2%. Before discovery and use of Insulin (1922) the mortality was 100%. Epidemiology DKA is reported in 2-5% of known type 1 diabetic patients in industrialized countries, while it occurs in 35-40% of such patients in Africa. DKA at the time of first diagnosis of diabetes mellitus is reported in only 2-3% in western Europe, but is seen in 95% of diabetic children in Sudan. Similar results were reported from other African countries . Consequences The latter observation is annoying because it implies the following: The late diagnosis of type 1 diabetes in many developing countries particularly in Africa. The late presentation of DKA, which is associated with risk of morbidity & mortality Death of young children with DKA undiagnosed or wrongly diagnosed as malaria or meningitis. Pathophysiology Secondary to insulin deficiency, and the action of counter-regulatory hormones, blood glucose increases leading to hyperglycemia and glucosuria. Glucosuria causes an osmotic diuresis, leading to water & Na loss. In the absence of insulin activity the body fails to utilize glucose as fuel and uses fats instead. This leads to ketosis. Pathophysiology/2 The excess of ketone bodies will cause metabolic acidosis, the later is also aggravated by Lactic acidosis caused by dehydration & poor tissue perfusion. Vomiting due to an ileus, plus increased insensible water losses due to tachypnea will worsen the state of dehydr Continue reading >>
Diabetic Ketoacidosis
Author: Osama Hamdy, MD, PhD; Chief Editor: Romesh Khardori, MD, PhD, FACP more... Diabetic ketoacidosis (DKA) is an acute, major, life-threatening complication of diabetes that mainly occurs in patients with type 1 diabetes, but it is not uncommon in some patients with type 2 diabetes. This condition is a complex disordered metabolic state characterized by hyperglycemia, ketoacidosis, and ketonuria. The most common early symptoms of DKA are the insidious increase in polydipsia and polyuria. The following are other signs and symptoms of DKA: Malaise, generalized weakness, and fatigability Nausea and vomiting; may be associated with diffuse abdominal pain, decreased appetite, and anorexia Rapid weight loss in patients newly diagnosed with type 1 diabetes History of failure to comply with insulin therapy or missed insulin injections due to vomiting or psychological reasons or history of mechanical failure of insulin infusion pump Altered consciousness (eg, mild disorientation, confusion); frank coma is uncommon but may occur when the condition is neglected or with severe dehydration/acidosis Signs and symptoms of DKA associated with possible intercurrent infection are as follows: Glaser NS, Marcin JP, Wootton-Gorges SL, et al. Correlation of clinical and biochemical findings with diabetic ketoacidosis-related cerebral edema in children using magnetic resonance diffusion-weighted imaging. J Pediatr. 2008 Jun 25. [Medline] . Umpierrez GE, Jones S, Smiley D, et al. Insulin analogs versus human insulin in the treatment of patients with diabetic ketoacidosis: a randomized controlled trial. Diabetes Care. 2009 Jul. 32(7):1164-9. [Medline] . [Full Text] . Herrington WG, Nye HJ, Hammersley MS, Watkinson PJ. Are arterial and venous samples clinically equivalent for the estimation Continue reading >>
Diabetic Ketoacidosis And Hyperosmolar Hyperglycemic State In Adults: Treatment
INTRODUCTION Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS, also known as hyperosmotic hyperglycemic nonketotic state [HHNK]) are two of the most serious acute complications of diabetes. They are part of the spectrum of hyperglycemia, and each represents an extreme in the spectrum. The treatment of DKA and HHS in adults will be reviewed here. The epidemiology, pathogenesis, clinical features, evaluation, and diagnosis of these disorders are discussed separately. DKA in children is also reviewed separately. (See "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Epidemiology and pathogenesis".) (See "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Clinical features, evaluation, and diagnosis".) Continue reading >>
Diabetic Ketoacidosis In A Patient With Type 1 Diabetes On Sodium-glucose Co-transporter-2 Inhibitorsa Case Report
US Endocrinology,2017;13(2):724 DOI: We describe a case of a 26-year-old female with long-standing type 1 diabetes (T1D), on multiple subcutaneous insulin injections, who had been taking empagliflozin for the past year. She was detected to have severe diabetic ketoacidosis (DKA) with relatively lower blood glucose values during hospitalisation for dengue fever. The factors that precipitated the DKA are discussed, along with the unique challenges in the management of her metabolic status. While sodium-glucose co-transporter-2 (SGLT2) inhibitors have several potential benefits as adjunctive add-on therapy to insulin in T1D, the evidence is limited to short-term studies. However, their off-label use is increasing and there have been concerns related to increased risk of diabetic ketoacidosis. At present, SGLT2 inhibitors are not approved for use in T1D, and the risks should be discussed at length with the patient. Keywords: Type 1 diabetes, diabetic ketoacidosis, euglycaemic diabetic ketoacidosis, sodium-glucose co-transporter-2 (SGLT2) inhibitors, empagliflozin Disclosure: Gagan Priya and Vishal Bhambri have nothing to declare in relation to this article. No funding was received in the publication of this article Open Access: This article is published under the Creative Commons Attribution Noncommercial License, which permits any non-commercial use, distribution, adaptation and reproduction provided the original author(s) and source are given appropriate credit. Received: September 20, 2017 Published Online: October 17, 2017 Correspondence: Gagan Priya, Department of Endocrinology, Fortis Hospital, Phase 8, Mohali 160059, India. E: [email protected] We report a case of diabetic ketoacidosis in a 26-year-old female with long-standing type 1 diabetes (T1D) who was on mult 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 >>
Diabetes Ketoacidosis
1. DIABETIC KETO-ACIDOSIS MANAGEMENT 2. INTRODUCTION HHS and DKA are not mutually exclusive but rather two conditions that both result from some degree of insulin deficiency. They can and often do occur simultaneously. In fact, one third of patients admitted for hyperglycemia exhibit characteristics of both HHS and DKA. 14th edition of Joslin's Diabetes Mellitus 3. DEFINITION DKA is defined as the presence of all three of the following: (i) Hyperglycemia (glucose >250 mg/dL) (ii) Ketosis, (iii) Acidemia (pH <7.3). 14th edition of Joslin's Diabetes Mellitus 4. PATHOPHYSIOLOGY Insulin Deficiency Glucose uptake Lipolysis Proteolysis Glycerol Free Fatty Acids Amino Acids Hyperglycemia Osmotic diuresis Ketogenesis Gluconeogenesis Glycogenolysis Dehydration Acidosis 14th edition of Joslin's Diabetes Mellitus 5. ROLE OF INSULIN Required for transport of glucose into: Muscle Adipose Liver Inhibits lipolysis Absence of insulin Glucose accumulates in the blood. Uses amino acids for gluconeogenesis Converts fatty acids into ketone bodies : Acetone, Acetoacetate, β-hydroxybutyrate. 6. DIABETIC KETOACIDOSIS PRECIPITATING EVENTS Infection(Pneumonia / UTI / Gastroenteritis / Sepsis) Inadequate insulin administration Infarction(cerebral, Drugs coronary, mesenteric, peripheral) (cocaine) Pregnancy. Harrison’s Principle of internal medicine 18th edition p2977 7. SYMPTOMS DKA PHYSICAL FINDINGS can be the first Dehydration/hypotension presentation. Tachypnea/kussmaul Nausea/vomiting Thirst/polyuria Abdominal pain Shortnessof Tachycardia breath respirations/respiratory distress Fruity odour in breath. Abdominal tenderness(may resemble acute pancreatitis or surgical abdomen) Lethargy/obtundati Continue reading >>
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 >>
Euglycemic Diabetic Ketoacidosis: A Diagnostic And Therapeutic Dilemma
Prashanth Rawla1, Anantha R Vellipuram2, Sathyajit S Bandaru3 and Jeffrey Pradeep Raj4[1] Department of Internal Medicine, Memorial Hospital of Martinsville and Henry County, Martinsville, Virginia, USA [2] Texas Tech University Health Sciences Center, El Paso, Texas, USA [3] Senior Research Associate, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA [4] Department of Pharmacology, St John’s Medical College, Bangalore, India Summary Euglycemic diabetic ketoacidosis (EDKA) is a clinical triad comprising increased anion gap metabolic acidosis, ketonemia or ketonuria and normal blood glucose levels <200 mg/dL. This condition is a diagnostic challenge as euglycemia masquerades the underlying diabetic ketoacidosis. Thus, a high clinical suspicion is warranted, and other diagnosis ruled out. Here, we present two patients on regular insulin treatment who were admitted with a diagnosis of EDKA. The first patient had insulin pump failure and the second patient had urinary tract infection and nausea, thereby resulting in starvation. Both of them were aggressively treated with intravenous fluids and insulin drip as per the protocol for the blood glucose levels till the anion gap normalized, and the metabolic acidosis reversed. This case series summarizes, in brief, the etiology, pathophysiology and treatment of EDKA. Euglycemic diabetic ketoacidosis is rare. Consider ketosis in patients with DKA even if their serum glucose levels are normal. High clinical suspicion is required to diagnose EDKA as normal blood sugar levels masquerade the underlying DKA and cause a diagnostic and therapeutic dilemma. Blood pH and blood or urine ketones should be checked in ill patients with diabetes regardless of blood glucose levels. Background Diabetic ket Continue reading >>
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Reference
This purpose of this talk is to overview the 2017 American Diabetes Association Standards of Medical Care in Diabetes. These Standards comprise all of the current and key clinical practice recommendations of the American Diabetes Association. [SLIDE] 2 Reference American Diabetes Association. Standards of medical care in diabetes—2014. Diabetes Care 2014;37(suppl 1):S1 A few notes on the Standards of Care: The Association funds development of the Standards of Care and all Association position statements out of its general revenues and does not use industry support for these purposes [CLICK] The slides are organized to correspond with sections within the 2017 Standards of Care. As we go through I’ll make note of where we are within the document. [CLICK] Though not every section in the document is represented, these slides do incorporate the most salient points from the Position Statement As with all Association position statements, the Standards of Care are reviewed and approved by the Association’s Board of Directors, which includes health care professionals, scientists, and lay people. [SLIDE] 3 These Standards of Care are revised annually by the ADA’s multidisciplinary Professional Practice Committee (PPC) [CLICK] For the 2017 revision, PPC members systematically searched Medline for human studies related to each subsection and published since 1 January 2016. [CLICK] Recommendations were revised based on new evidence or, in some cases, to clarify the prior recommendations or match the strength of the word to the strength of the evidence [CLICK] A table linking the changes in the recommendations to new evidence can be reviewed at professional.diabetes.org/SOC (Standards of Care) [CLICK] The Association and the Professional Practice Committee Continue reading >>
Trends In Diabetic Ketoacidosis Hospitalizations And In-hospital Mortality United States, 20002014
Trends in Diabetic Ketoacidosis Hospitalizations and In-Hospital Mortality United States, 20002014 Diabetic ketoacidosis (DKA) is a life-threatening complication of diabetes, a disease that affects approximately 30 million persons in the United States. DKA is more common among persons with type 1 diabetes. After a slight decline during 20002009, hospitalizations for DKA increased in the United States during 20092014 among all age groups and were highest among persons aged <45 years. Concurrently, in-hospital case-fatality rates among persons with DKA consistently decreased from 2000 to 2014. What are the implications for public health practice? DKA is a life-threatening but avoidable complication of diabetes. Prevention measures, such as diabetes self-management education, might help reverse the increasing trend in DKA, especially in persons aged <45 years who have the highest DKA rates. Diabetes is a common chronic condition and as of 2015, approximately 30 million persons in the United States had diabetes (23 million with diagnosed and 7 million with undiagnosed) (1). Diabetic ketoacidosis (DKA) is a life-threatening but preventable complication of diabetes characterized by uncontrolled hyperglycemia (>250 mg/dL), metabolic acidosis, and increased ketone concentration that occurs most frequently in persons with type 1 diabetes (2). CDCs United States Diabetes Surveillance System* (USDSS) indicated an increase in hospitalization rates for DKA during 20092014, most notably in persons aged <45 years. To explore this finding, 20002014 data from the Agency for Healthcare Research and Qualitys National Inpatient Sample (NIS) were assembled to calculate trends in DKA hospitalization rates and in-hospital case-fatality rates. Overall, age-adjusted DKA hospitalization rates d Continue reading >>
Treatment Of Diabetic Ketoacidosis (dka)/hyperglycemic Hyperosmolar State (hhs): Novel Advances In The Management Of Hyperglycemic Crises (uk Versus Usa)
Go to: Diabetic Ketoacidosis Prior to the discovery and isolation of insulin in 1922 by Banting and Best, type 1 diabetes was universally fatal within a few months of initial diagnosis. Once mass production was started, the challenge to those early pioneers of insulin treatment was learning how to use this new wonder drug, e.g., how much to give and how often to give it, in order to treat the hyperglycemia without raising the inherent risk of hypoglycemia. In 1945, Howard Root in Boston described how they had improved the outcomes for people with diabetic ketoacidosis (DKA), reducing mortality to 12% by 1940 and to 1.6% by 1945 using high doses of insulin—giving an average of 83 units within the first 3 h of treatment in 1940 and 216 units by 1945 [3]. They described how in 1945, they used an average of 287 units in the first 24 h, but this ranged from 50 to 1770 units [3]. In Birmingham, UK, high-dose insulin was also being used with similar success—doses varying depending on the degree of consciousness, with those unarousable on admission given doses between 500 and 1400 units per 24 h [4]. DKA remains a medical emergency; over time, mortality has continued to fall but remains a significant risk, especially amongst the young, socially isolated and when care provision is fragmented [5•, 6•]. Overall, the diagnosis and treatment of DKA are very similar in the UK and USA with a few differences. The UK has separate guidelines on the management of DKA [7], while the USA has a position statement on DKA and HHS that was updated in 2009 [8]. The UK guideline differs in several ways from the US position statement. The concept of low-dose intravenous insulin was established in the late 1960s and early 1970s by teams on both sides of the Atlantic. The UK championed the u Continue reading >>
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 >>
