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Dka In Pregnancy Algorithm

Emdocs.net Emergency Medicine Educationem@3am: Diabetic Ketoacidosis - Emdocs.net - Emergency Medicine Education

Emdocs.net Emergency Medicine Educationem@3am: Diabetic Ketoacidosis - Emdocs.net - Emergency Medicine Education

Author: Brit Long, MD (@long_brit, EM Attending Physician, San Antonio, TX) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) Welcome to EM@3AM, an emDOCs series designed to foster your working knowledge by providing an expedited review of clinical basics. Well keep it short, while you keep that EM brain sharp. A 37-year-old female presents with dysuria, polyuria, polydipsia, and lightheadedness. She has a history of insulin-dependent diabetes. She has not checked her blood glucose at home within the last week, as she ran out of her testing strips. She denies vomiting, but has had significant nausea and suprapubic pain. Initial VS include T 37.2C, HR 112, BP 110/61, RR 28, SpO2 97% RA. Exam reveals dry oral mucosa and suprapubic tenderness. No CVA tenderness is elicited, and the rest of the exam is normal. ECG reveals sinus tachycardia, but POC glucose is 422 mg/dL. What is the patients diagnosis? Whats the next step in your evaluation and treatment? Definition: A state of hyperglycemia and acidemia due to insulin deficiency: glucose > 250 mg/dL, acidosis (pH < 7.3), ketosis. Hyperglycemia: Insulin deficiency leads to elevated serum glucose, which results in osmotic diuresis and electrolyte depletion (Na, Mg, Ca, Ph). Acidosis: Lipolysis and ketoacid accumulation results in metabolic acidemia (with elevated anion gap). Inability to metabolize glucose leads to fatty acid breakdown and ketone production, which includes acetoacetate and beta-hydroxybutyrate. Dehydration results in activation of renin angiotensin aldosterone system and further osmotic diuresis. Background: Incidence is approximately 10,000 cases per year in the U.S., with mortality approaching 5%. However, before insulin administration, mortality reached Continue reading >>

Diabetic Ketoacidosis In Pregnancy.

Diabetic Ketoacidosis In Pregnancy.

Abstract Pregnancies complicated by diabetic ketoacidosis are associated with increased rates of perinatal morbidity and mortality. A high index of suspicion is required, because diabetic ketoacidosis onset in pregnancy can be insidious, usually at lower glucose levels, and often progresses more rapidly as compared with nonpregnancy. Morbidity and mortality can be reduced with early detection of precipitating factors (ie, infection, intractable vomiting, inadequate insulin management or inappropriate insulin cessation, β-sympathomimetic use, steroid administration for fetal lung maturation), prompt hospitalization, and targeted therapy with intensive monitoring. A multidisciplinary approach including a maternal-fetal medicine physician, medical endocrinology specialists familiar with the physiologic changes in pregnancy, an obstetric anesthesiologist, and skilled nursing is paramount. Management principles include aggressive volume replacement, initiation of intravenous insulin therapy, correction of acidosis, correction of electrolyte abnormalities and management of precipitating factors, as well as monitoring of maternal-fetal response to treatment. When diabetic ketoacidosis occurs after 24 weeks of gestation, fetal status should be continuously monitored given associated fetal hypoxemia and acidosis. The decision for delivery can be challenging and must be based on gestational age as well as maternal-fetal responses to therapy. The natural inclination is to proceed with emergent delivery for nonreassuring fetal status that is frequently present during the acute episode, but it is imperative to correct the maternal metabolic abnormalities first, because both maternal and fetal conditions will likewise improve. Prevention strategies should include education of diabet Continue reading >>

Diabetic Ketoacidosis In Pregnancy

Diabetic Ketoacidosis In Pregnancy

Episodes of diabetic ketoacidosis (DKA) can represent a life-threatening emergency for mother and fetus. The cornerstones of treatment of DKA are aggressive fluid replacement and insulin administration while ascertaining which precipitating factors brought about the current episode of DKA, and then treating accordingly to mitigate those factors. The incidence of DKA and factors unique to pregnancy are discussed in this article, along with the effects of the disease process on pregnancy. Clinical presentation, diagnosis, and treatment modalities are covered in detail to offer ideas to improve maternal and fetal outcome. Continue reading >>

Diabetic Ketoacidosis In Pregnancy | Obstetric Intensive Care Manual, 4e | Accessobgyn | Mcgraw-hill Medical

Diabetic Ketoacidosis In Pregnancy | Obstetric Intensive Care Manual, 4e | Accessobgyn | Mcgraw-hill Medical

Despite recent advances in the evaluation and medical treatment of diabetes in pregnancy, diabetic ketoacidosis (DKA) remains a matter of significant concern. The fetal loss rate in most contemporary series has been estimated to range from 10% to 25%. Fortunately, since the advent and implementation of insulin therapy, the maternal mortality rate has declined to 1% or less. In order to favorably influence the outcome in these high-risk patients, it is imperative that the obstetrician/provider be familiar with the basics of the pathophysiology, diagnosis, and treatment of DKA in pregnancy. DKA is characterized by hyperglycemia and accelerated ketogenesis. Both a lack of insulin and an excess of glucagon and other counter-regulatory hormones significantly contribute to these problems and their resultant clinical manifestations. Glucose normally enters the cell secondary to the effects of insulin. The cell then may use glucose for nutrition and energy production. When insulin is lacking, glucose fails to enter the cell. The cell responds to this starvation by facilitating the release of counter-regulatory hormones, including glucagon, catecholamines, and cortisol. These counter-regulatory hormones are responsible for providing the cell with an alternative substrate for nutrition and energy production. By the process of gluconeogenesis, fatty acids from adipose tissue are broken down by hepatocytes to ketones (acetone, acetoacetate, and -hydroxybutyrate [BHB] = ketone bodies), which are then used by the body cells for nutrition and energy production ( Fig. 11-1 ). The lack of insulin also contributes to increased lipolysis and decreased reutilization of free fatty acids, thereby providing more substrate for hepatic ketogenesis. A basic review of the biochemistry involving 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 >>

Managing Severe Preeclampsia And Diabetic Ketoacidosis In Pregnancy

Managing Severe Preeclampsia And Diabetic Ketoacidosis In Pregnancy

US Pharm. 2010;35(9):HS-2-HS-8. Pregnancy is associated with increased levels of emotional and physical stress. Women with preexisting conditions such as hypertension and diabetes require intense prenatal monitoring by health care professionals. Pharmacists in direct contact with patients can play an integral role in identifying signs and symptoms that require immediate care. Two conditions that require emergent treatment in pregnant women are severe preeclampsia and diabetic ketoacidosis. SEVERE PREECLAMPSIA Hypertensive disorders can affect 6% to 8% of women and increase the risk of morbidity and mortality in both the expectant mother and the unborn child.1,2 Hypertension in pregnancy is divided into four categories: chronic hypertension, gestational hypertension, preeclampsia, and preeclampsia superimposed on chronic hypertension. The focus in this article is on severe preeclampsia, but a brief discussion of preeclampsia is warranted. Preeclampsia, a pregnancy-specific syndrome of unknown etiology, is a multiorgan disease process characterized by the development of hypertension and proteinuria after 20 weeks' gestation.1,2 See TABLE 1 for diagnostic criteria.1,2 History of antiphospholipid antibody syndrome, chronic hypertension, chronic renal disease, elevated body-mass index, age 40 years or older, multiple gestation, nulliparity, preeclampsia in a previous pregnancy, and pregestational diabetes mellitus increase a woman's risk of preeclampsia.1 Preeclampsia is classified as mild or severe based on the degree of hypertension, the level of proteinuria, and the presence of symptoms resulting from the involvement of the kidneys, brain, liver, and cardiovascular system. The incidence of severe preeclampsia is 0.9% in the United States.3 Severe preeclampsia is associate Continue reading >>

Updated Feb 2017 J Clayton

Updated Feb 2017 J Clayton

NUH Management of Diabetic Ketoacidosis in Adults (18 years old & over) (Please see the Paediatric guidelines for patients under 18 years) If in doubt, call someone more senior. KETOACIDOSIS CAN KILL. Use in conjunction with the NUH pathway of care for DKA in adults (insulin prescription, administration and monitoring chart). 1. DIAGNOSIS All three required 1. Raised blood glucose>11mmol /L or known diabetes 2. Capillary ketones > 3 mmol/L (or Ketones >2+ in urine) 3. Venous pH < 7.35 or venous bicarb < 15mmol/L 2. ESSENTIAL INVESTIGATIONS Arterial puncture NOT routinely needed  U+E, creatinine, blood glucose  Venous blood gas for bicarbonate, potassium and pH (analyse on machine on B3, ED, HDU, ITU)  ECG/CXR/MSU/blood cultures/pregnancy test depending on clinical suspicion Raised WCC and serum amylase are common in DKA and do not usually suggest pancreatitis. 4. IMMEDIATE TREATMENT START IN EMERGENCY DEPT / ASSESSMENT UNIT OR THEIR CURRENT LOCATION. DELAY IN STARTING TREATMENT MAY BE FATAL. 1. Insert venflon 2. 1L 0.9% sodium chloride infusion over 1hr if systolic BP>90 (If systolic BP<90 give repeated boluses of 500ml 0.9% sodium chloride over 10-15 minutes) 3. Start IV insulin infusion: 50 units human soluble (ACTRAPID®) insulin added to 49.5 mls 0.9% sodium chloride to give a 1 unit/ml solution via syringe driver at 0.1 units/ kg / hr (estimated or actual weight) 3. SEVERITY (Venous bicarbonate or pH) >14 mmol/l or pH >7.3 Mild 10-14 mmol/l or pH 7.1-7.3 Moderate < 10 mmol/l or pH <7.1 Severe 5. TRANSFER NO PATIENT WITH DKA SHOULD BE TRANSFERRED BETWEEN HOSPITALS URGENT CRITICAL CARE/HDU REVIEW if any of: Venous bicarbonate < 10 mmol/l or pH<7.1, drowsy (P or U on AVPU), fluid balance problems, pregnancy, co morbidities, sats<94% on 40% O2, p Continue reading >>

Chapter 11: Diabetic Ketoacidosis In Pregnancy

Chapter 11: Diabetic Ketoacidosis In Pregnancy

Despite recent advances in the evaluation and medical treatment of diabetes in pregnancy, diabetic ketoacidosis (DKA) remains a matter of significant concern. The fetal loss rate in most contemporary series has been estimated to range from 10% to 25%. Fortunately, since the advent and implementation of insulin therapy, the maternal mortality rate has declined to 1% or less. In order to favorably influence the outcome in these high-risk patients, it is imperative that the obstetrician/provider be familiar with the basics of the pathophysiology, diagnosis, and treatment of DKA in pregnancy. DKA is characterized by hyperglycemia and accelerated ketogenesis. Both a lack of insulin and an excess of glucagon and other counter-regulatory hormones significantly contribute to these problems and their resultant clinical manifestations. Glucose normally enters the cell secondary to the effects of insulin. The cell then may use glucose for nutrition and energy production. When insulin is lacking, glucose fails to enter the cell. The cell responds to this starvation by facilitating the release of counter-regulatory hormones, including glucagon, catecholamines, and cortisol. These counter-regulatory hormones are responsible for providing the cell with an alternative substrate for nutrition and energy production. By the process of gluconeogenesis, fatty acids from adipose tissue are broken down by hepatocytes to ketones (acetone, acetoacetate, and β-hydroxybutyrate [BHB] = ketone bodies), which are then used by the body cells for nutrition and energy production (Fig. 11-1). The lack of insulin also contributes to increased lipolysis and decreased reutilization of free fatty acids, thereby providing more substrate for hepatic ketogenesis. A basic review of the biochemistry involving D Continue reading >>

Clinical Variables Associated With Diabetic Ketoacidosis During Pregnancy.

Clinical Variables Associated With Diabetic Ketoacidosis During Pregnancy.

Clinical variables associated with diabetic ketoacidosis during pregnancy. 1. Department of Obstetrics and Gynecology, State University of New York, Buffalo 14222. The Journal of Reproductive Medicine, 01 Nov 1991, 36(11):797-800 Share this article Share with emailShare with twitterShare with linkedinShare with facebook A retrospective review was conducted of all women with diabetic pregnancies admitted in diabetic ketoacidosis (DKA) to hospitals affiliated with the State University of New York at Buffalo between 1980 and 1990. The experience was combined with a literature review of similar patients described between 1970 and 1990, for a total of 37 admissions for DKA during pregnancy. Emesis and the use of beta-sympathomimetic drugs were considered etiologic in 57% of cases, while patient noncompliance and physician management errors were considered etiologic in 24% and contributory in 16%. Thirty percent of patients admitted with emesis had a prepregnancy history of diabetic gastroenteropathy, thus identifying that group as at particularly high risk for DKA. In the context of modern management, the causes of DKA in pregnancy are related uniquely to pregnancy, and the disorder is largely preventable during pregnancy. Continue reading >>

Diabetes In Pregnancy (nice Clinical Guideline 3)

Diabetes In Pregnancy (nice Clinical Guideline 3)

This guideline was produced by the National Collaborating Centre for Women’s and Children’s Health (NCC-WCH) on behalf of the National Institute of Health and Care Excellence (NICE). The guideline focuses on areas where additional or different care should be offered to women with diabetes and their newborn babies. Where the evidence supports it, the guideline makes separate recommendations for women with pre‑existing diabetes and women with gestational diabetes. Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Authors Runa Acharya, MD, University of Iowa-Des Moines Internal Medicine Residency Program at UnityPoint Health, Des Moines, IA Udaya M. Kabadi, MD, FACP, FRCP(C), FACE, Veteran Affairs Medical Center and Broadlawns Medical Center, Des Moines, IA; Des Moines University of Osteopathic Medicine, Iowa City; and University of Iowa Carver College of Medicine, Iowa City; Adjunct Professor of Medicine and Endocrinology, University of Iowa, Iowa City, and Des Moines University, Des Moines Peer Reviewer Jay Shubrook, DO, FAAFP, FACOFP, Professor, Primary Care Department, Touro University, College of Osteopathic Medicine, Vallejo, CA Statement of Financial Disclosure To reveal any potential bias in this publication, and in accordance with Accreditation Council for Continuing Medical Education guidelines, Dr. Kabadi (author) reports he is a consultant and on the speakers bureau for Sanofi. Dr. Shubrook (peer reviewer) reports he receives grant/research support from Sanofi and is a consultant for Eil Lilly, Novo Nordisk, and Astra Zeneca. Dr. Acharya (author) reports no financial relationships relevant to this field of study. Continue reading >>

Diabetic Ketoacidosis In Pregnancy

Diabetic Ketoacidosis In Pregnancy

saveSave Diabetic Ketoacidosis in Pregnancy For Later saveSave Diabetic Ketoacidosis in Pregnancy For Later Jason A. Parker, MDa, Deborah L. Conway, MDa,* Department of Obstetrics and Gynecology, Division of Maternal-Fetal Medicine, The University of Texas Health Science Center in San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78229, USA Diabetic ketoacidosis (DKA) is a disease process involving numerous pathophysiologic changes that can be markedly exaggerated in the pregnant state. Episodes of DKA are infrequent in the general population and even more so in pregnancy. Nonetheless, DKA may represent a life-threatening event for the mother and her fetus. The incidence of DKA and factors unique to pregnancy are discussed in this article, along with the eects of the disease process on pregnancy. Clinical presentation, diagnosis, and treatment modalities are covered in detail to oer data to improve maternal and fetal outcome. The reported incidence of DKA outside of pregnancy ranges from 4.6 to 8 episodes per 1000 patients annually [1]. The overall incidence of DKA in pregnancies complicated by diabetes is dicult to ascertain. Numerous review articles and retrospective studies have found the incidence to range from 1% to 10%, and the overall prevalence of DKA during pregnancy and fetal loss associated with DKA have fallen signicantly in recent years. This trend is likely secondary to prenatal counseling (with a goal of optimal glucose control before pregnancy) and improved understanding and management of the acute event. Cousins [2] reported the incidence of DKA during pregnancy to be 9.3% in a group of 1508 patients studied between 1965 and 1985. More recent retrospective studies by Rodgers and Rodgers [3] and Cullen and colleagues [4] found an incidence of DKA in p Continue reading >>

Diabetic Ketoacidosistreatment & Management

Diabetic Ketoacidosistreatment & Management

Diabetic KetoacidosisTreatment & Management Author: Osama Hamdy, MD, PhD; Chief Editor: Romesh Khardori, MD, PhD, FACP more... 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: Correction of fluid loss with intravenous fluids Correction of electrolyte disturbances, particularly potassium loss Treatment of concurrent infection, if present 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 ultrashort-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 Continue reading >>

Diabetes In Pregnancy: Management Of Diabetes And Its Complications From Preconception To The Postnatal Period.

Diabetes In Pregnancy: Management Of Diabetes And Its Complications From Preconception To The Postnatal Period.

National Collaborating Centre for Women's and Children's Health Note from the National Guideline Clearinghouse (NGC): This guideline update was developed by the National Collaborating Centre for Women's and Children's Health on behalf of the National Institute for Health and Care Excellence (NICE). See the "Availability of Companion Documents" field for the full version of this guidance and relevant appendices. Recommendations are marked as [new 2015], [2015], [2008] or [2008, amended 2015]: [new 2015] indicates that the evidence has been reviewed and the recommendation has been added or updated [2015] indicates that the evidence has been reviewed but no change has been made to the recommended action [2008] indicates that the evidence has not been reviewed since 2008 [2008, amended 2015] indicates that the evidence has not been reviewed since 2008, but either changes have been made to the recommendation wording that change the meaning or NICE has made editorial changes to the original wording to clarify the action to be taken. The wording used in the recommendations in this guideline (for example words such as 'offer' and 'consider') denotes the certainty with which the recommendation is made (the strength of the recommendation) and is defined at the end of the "Major Recommendations" field. This guideline refers frequently to circulating glucose concentrations as 'blood glucose'. A lot of the evidence linking specific circulating glucose concentrations with particular outcomes uses 'plasma' rather than 'blood' glucose. In addition, patient-held glucose meters (which use capillary blood samples) and monitoring systems are all calibrated to plasma glucose equivalents. However, the term 'blood glucose monitoring' is in very common use, so in this guideline the term 'bloo Continue reading >>

Diabetes Ketoacidosis

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 >>

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