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Dka In Pregnancy Algorithm

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 >>

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 >>

Ketoacidosis In Diabetic Pregnancy

Ketoacidosis In Diabetic Pregnancy

Diabetic ketoacidosis (DKA) is a serious medical and obstetrical emergency previously considered typical of type 1 diabetes but now reported also in type 2 and GDM patients. Although it is a fairly rare condition, DKA in pregnancy can compromise both fetus and mother. Metabolic changes occurring during pregnancy predispose to DKA in fact it can develop even in setting of normoglycemia. This article will provide the reader with information regarding the pathophysiology underlying DKA, in particular euglycemic DKA, and will provide information regarding all possible effects of ketones on the fetus. 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 >>

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 >>

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 >>

Diabetic Ketoacidosis In Pregnancy

Diabetic Ketoacidosis In Pregnancy

Diagnosis of DKA: � Initial STAT labs include • CBC with diff • Serum electrolytes • BUN • Creatinine • Glucose • Arterial blood gases • Bicarbonate • Urinalysis • Lactate • Serum ketones • Calculation of the Anion Gap � serum anion gap = serum sodium – (serum chloride + bicarbonate) • Electrocardiogram Treatment Protocol for Diabetic Ketoacidosis Reviewed 5/2/2017 2 Updated 05/02/17 DKA Diagnostic Criteria: � Blood glucose >250 mg/dl � Arterial pH <7.3 � Bicarbonate ≤18 mEq/l � Anion Gap Acidosis � Moderate ketonuria or ketonemia 1. Start IV fluids (1 L of 0.9% NaCl per hr initially) 2. If serum K+ is <3.3 mEq/L hold insulin � Give 40 mEq/h until K ≥ 3.3 mEq/L 3. Initiate DKA Order Set Phase I (*In PREGNANCY utilize OB DKA order set) 4. Start insulin 0.14 units/kg/hr IV infusion (calculate dose) RN will titrate per DKA protocol Insulin Potassium Bicarbonate IVF Look for the Cause - Infection/Inflammation (PNA, UTI, pancreatitis, cholecystitis) - Ischemia/Infarction (myocardial, cerebral, gut) - Intoxication (EtOH, drugs) - Iatrogenic (drugs, lack of insulin) - Insulin deficiency - Pregnancy DKA/HHS Pathway Phase 1 (Adult) Approved by Diabetes Steering Committee, MMC, 2015, Revised DKA Workgroup 1_2016 Initiate and continue insulin gtt until serum glucose reaches 250 mg/dl. RN will titrate per protocol to achieve target. When sugar < 250 mg/dl proceed to DKA Phase II *In PREGNANCY when sugar <200 proceed to OB DKA Phase II *PREGNANCY � Utilize OB DKA order set Phase 1 � When glucose reaches 200mg/dL, Initiate OB DKA Phase 2 � Glucose goals 100-150mg/dL OB DKA Phase 2 Determine hydration status Hypovolemic shock Mild hypotensio Continue reading >>

Diabetes In Pregnancy: Management From Preconception To The Postnatal Period

Diabetes In Pregnancy: Management From Preconception To The Postnatal Period

If you have type 1 diabetes, you should be given ketone testing strips and a monitor. Your care team should advise you to test the ketone levels in your blood if your blood glucose is too high (known as hyperglycaemia) or if you are unwell. This is because you are at risk of a serious condition called diabetic ketoacidosis (DKA). People with type 1 diabetes are at higher risk of DKA (although anyone with diabetes can get it). If you have any form of diabetes, your care team should advise you to get urgent medical advice if you have hyperglycaemia or you are feeling unwell, to make sure you don't have DKA. Your ketone levels should be checked as soon as possible. If you are thought to have DKA you should be admitted straight away to a unit where you can get specialist care. 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 >>

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 >>

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 >>

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 >>

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 >>

Managing Diabetic Ketoacidosis In Pregnancy

Managing Diabetic Ketoacidosis In Pregnancy

Sir, Diabetic ketoacidosis (DKA) is a potentially life-threatening condition in pregnancy,[1] affecting 0.5-3% of diabetic pregnancies.[2] We describe a woman who developed DKA due to insulin pump malfunction. A 35-year-old nulliparous diabetic, usually well-managed with a subcutaneous insulin pump, presented at 33 weeks gestation with malaise, vomiting, Kussmaul breathing and uterine contractions. Vital signs were, blood pressure 140/70 mmHg, heart rate 110 beats/min, respiratory rate 25 breaths/min and temperature 37°C. Laboratory tests were abnormal [Table 1]. The fetal heart trace showed poor variability, with late decelerations. In the intensive care unit, she received intravenous 0.9% normal saline (2 L over 3 h), then plasmalyte solution at 250 ml/h); insulin 10 u/h; and intravenous potassium. Her clinical and metabolic condition improved over 24 h [Table 1] and both contractions and late decelerations resolved. She was later discharged with a new subcutaneous insulin pump and was delivered uneventfully by elective cesarean section at 37 weeks. Pregnancy constitutes a state of insulin resistance, accelerated starvation and respiratory alkalosis with compensatory renal bicarbonate excretion, predisposing to DKA.[2] Increased insulin resistance and/or inadequate insulin[3] may lead to hormonal-induced release of alternative energy substrates,[1] with uncontrolled hyperglycemia, dehydration, loss of electrolytes (osmotic diuresis), ketosis and metabolic acidosis.[2] The physiological response is a self-perpetuating chain of events, involving increased respiratory rate and depth (Kussmaul respiration) and compensatory low serum bicarbonate, producing an abnormal high anion gap[1] [Figures 1 and 2]. Fetal distress follows compromised uteroplacental perfusion (materna Continue reading >>

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