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Dka Vital Signs

Vital Sign Triage To Rule Out Diabetic Ketoacidosis And Non-ketotic Hyperosmolar Syndrome In Hyperglycemic Patients.

Vital Sign Triage To Rule Out Diabetic Ketoacidosis And Non-ketotic Hyperosmolar Syndrome In Hyperglycemic Patients.

Abstract AIMS: To develop a prediction algorithm to rule out diabetic ketoacidosis (DKA) and non-ketotic hyperosmolar syndrome (NKHS) based on vital signs for early triage of patients with diabetes. METHODS: The subjects were consecutive adult diabetic patients with hyperglycemia (blood glucose >or=250mg/dl) who presented at an emergency department. Based on a derivation sample (n=392, 70% of 544 patients at a hospital in Okinawa), recursive partitioning analysis was used to develop a tree-based algorithm. Validation was conducted using the other 30% of the patients in Okinawa (n=152, internal validation) and patients at a hospital in Tokyo (n=95, external validation). RESULTS: Three risk groups for DKA/NKHS were identified: a high-risk group of patients with glucose >400mg/dl or systolic blood pressure <100mmHg; a low risk group of patients with glucose or=100mmHg, pulse Continue reading >>

Diabetic Ketoacidosis: “sneaky” Triggers And Clinical Pearls

Diabetic Ketoacidosis: “sneaky” Triggers And Clinical Pearls

Authors: Catherine Reynolds, MD (EM Resident Physician, UT Houston), Kathryn Fisher, MD (EM Resident Physician, UT Houston), and Hilary Fairbrother, MD (EM Attending Physician, UT Houston) // Edited by: Alex Koyfman, MD (@EMHighAK) and Brit Long, MD (@long_brit) Clinical Case #1: The patient is a 45-year-old male with history of type 2 DM and HTN who presents to the emergency department with diffuse abdominal pain, nausea, and vomiting for two days. The patient reports that he was recently started on Invokana (canagliflozin) about two weeks ago for his diabetes, and prior to that he was managing his sugars with diet and exercise alone. The patient has had difficulty keeping any food down over the last two days, but denies shortness of breath, chest pain, or fever. He reports his vomit is non-bilious and non-bloody. His initial finger stick is 84 mg/dL, and your intern states that he “knows that this is not DKA” as the serum glucose is normal. Vital signs showed RR 28, HR 110, BP 152/86, SpO2 98% on room air, T 98.4 F. Labs on presentation reveal a Na of 132 mmol/L, K of 5 mmol/L, Cl of 98 mmol/L, bicarbonate of 10 mmol/L, glucose of 84 mg/dL, and venous pH of 7.1. Venous lactate is within normal limits, and serum beta-hydroxybutyrate is positive. The patient is started on dextrose-containing fluids, an insulin drip, and admitted to the ICU for DKA. What was the cause of the patient’s euglycemic DKA? Clinical Case #2: The patient is a 62-year-old male with a history of DM, CAD, HTN, HLD, an NSTEMI, and 2 subsequent cardiac stents. He presents to the ED with diffuse abdominal pain, nausea, vomiting, and diarrhea for two days. The patient is on Humalog and Lantus but he hasn’t taken the medications over the last two days because he hasn’t been eating. He denies s Continue reading >>

Diabetic Ketoacidosis (dka) Myths

Diabetic Ketoacidosis (dka) Myths

Recently, I was asked to give a lecture to both my residents and nurses at the University of Texas Health Science Center at San Antonio (UTHSCSA) on some common DKA myths. Now this topic was originally covered by my good friend Anand Swaminathan on multiple platforms and I did ask his permission to create this blogpost with the idea of improving patient care and wanted to express full disclosure of that fact. I specifically covered four common myths that I still see people doing in regards to DKA management: We should get ABGs instead of VBGs After Intravenous Fluids (IVF), Insulin is the Next Step Once pH <7.1, Patients Need Bicarbonate Therapy We Should Bolus Insulin before starting the infusion DKA Myths Case: 25 y/o female with PMH of Type I DM who presents via EMS with AMS. Per EMS report, the patient ran out of her insulin 3 days ago….. Vital Signs: BP 86/52 HR 136 RR 30 O2Sat 97% on room air Temp 99.1 Accucheck: CRITICAL HIGH EMS was not able to establish IV access, so decided to just bring her to the ED due to how sick she looks. Your nurses are on point today and get you two large bore 18G IVs and start to draw blood work to send to the lab. You state I need a blood gas, and the nurse turns to you and asks do you need an ABG or VBG? Myth #1: We should get ABGs instead of VBGs in DKA So you do a literature review and come across two studies that specifically look at ABG vs VBG in an ED population: Study #1: Kelly AM et al. Review Article – Can Venous Blood Gas Analysis Replace Arterial in Emergency Medical Care. Emery Med Australas 2010; 22: 493 – 498. PMID: 21143397 For pH, 3 studies of patients with DKA (265 patients) were reviewed showing a weighted mean difference of 0.02 pH units. Only one study, which was the largest study (200 patients) reported 95% Continue reading >>

Cc: Test 3 - Dka And Hhns Case Study

Cc: Test 3 - Dka And Hhns Case Study

Sort DKA Case Study Mr. Jones, a 65 year old male, is admitted to the Emergency Department in an unconscious state. His family tells you he has a history of IDDM. Mr. Jones' daughter says that he had had the flu and has been unable to eat or drink very much for several days. She is not sure whether he has taken insulin in the last 24 hours. On admission, his vital signs are: Temperature 101.8 degrees F. Pulse 120/minute, weak and thready Respiration 22/minute deep (with fruity breath odor) Blood pressure 64/42 mmHg A basic metabolic profile, complete blood counts, and arterial blood gases are drawn. The nurse initiates an IV infusion of normal saline. ... Does insulin Stimulate or Inhibit each of the following processes? ____ glucose uptake by the cells ____ glycogenolysis ____ gluconeogenesis ____ glycogenesis ____ lipolysis ____ protein catabolism Stimulate Inhibit Inhibit List 5 counterregulatory hormones and their impact on this diabetic emergency. Blood glucose- Serum osmolality- BUN- Potassium- Arterial pH- Arterial pCO2- glucagon - glucagon is a hormone produced by the pancreas that, along with insulin, controls the level of glucose in the blood. Glucagon has the opposite effect of insulin. It increases the glucose levels in blood. Glucagon, the drug, is a synthetic (man-made) version of human glucagon and is manufactured by genetic engineering using the bacteria Escherichia coli. Glucagon is used to increase the blood glucose level in severe hypoglycemia (low blood glucose). Glucagon is a glucose-elevating drug. epinephrine - cortisol - one major function of cortisol is the regulation of glucose concentration. It increases blood glucose through stimulation of hepatic glucogenesis (conversion of amino acids to glucose) and inhibiting protein synthesis norepinephr Continue reading >>

Management Of Diabetic Ketoacidosis In Adults

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 >>

The Management Of Diabetic Ketoacidosis In Children

The Management Of Diabetic Ketoacidosis In Children

, Volume 1, Issue2 , pp 103120 | Cite as The management of diabetic ketoacidosis in children The object of this review is to provide the definitions, frequency, risk factors, pathophysiology, diagnostic considerations, and management recommendations for diabetic ketoacidosis (DKA) in children and adolescents, and to convey current knowledge of the causes of permanent disability or mortality from complications of DKA or its management, particularly the most common complication, cerebral edema (CE). DKA frequency at the time of diagnosis of pediatric diabetes is 10%70%, varying with the availability of healthcare and the incidence of type 1 diabetes (T1D) in the community. Recurrent DKA rates are also dependent on medical services and socioeconomic circumstances. Management should be in centers with experience and where vital signs, neurologic status, and biochemistry can be monitored with sufficient frequency to prevent complications or, in the case of CE, to intervene rapidly with mannitol or hypertonic saline infusion. Fluid infusion should precede insulin administration (0.1 U/kg/h) by 12 hours; an initial bolus of 1020 mL/kg 0.9% saline is followed by 0.45% saline calculated to supply maintenance and replace 5%10% dehydration. Potassium (K) must be replaced early and sufficiently. Bicarbonate administration is contraindicated. The prevention of DKA at onset of diabetes requires an informed community and high index of suspicion; prevention of recurrent DKA, which is almost always due to insulin omission, necessitates a committed team effort. adolescentscerebral edemachildrencomplicationsdiabetic ketoacidosisfluid replacementhypokalemiamanagementpreventionrecurrent DKA This article is published with open access at Springerlink.com Diabetic ketoacidosis (DKA) is bioche Continue reading >>

Management Of Diabetic Ketoacidosis In Children And Adolescents

Management Of Diabetic Ketoacidosis In Children And Adolescents

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

Diabetic Ketoacidosis - Symptoms

Diabetic Ketoacidosis - Symptoms

A A A Diabetic Ketoacidosis Diabetic ketoacidosis (DKA) results from dehydration during a state of relative insulin deficiency, associated with high blood levels of sugar level and organic acids called ketones. Diabetic ketoacidosis is associated with significant disturbances of the body's chemistry, which resolve with proper therapy. Diabetic ketoacidosis usually occurs in people with type 1 (juvenile) diabetes mellitus (T1DM), but diabetic ketoacidosis can develop in any person with diabetes. Since type 1 diabetes typically starts before age 25 years, diabetic ketoacidosis is most common in this age group, but it may occur at any age. Males and females are equally affected. Diabetic ketoacidosis occurs when a person with diabetes becomes dehydrated. As the body produces a stress response, hormones (unopposed by insulin due to the insulin deficiency) begin to break down muscle, fat, and liver cells into glucose (sugar) and fatty acids for use as fuel. These hormones include glucagon, growth hormone, and adrenaline. These fatty acids are converted to ketones by a process called oxidation. The body consumes its own muscle, fat, and liver cells for fuel. In diabetic ketoacidosis, the body shifts from its normal fed metabolism (using carbohydrates for fuel) to a fasting state (using fat for fuel). The resulting increase in blood sugar occurs, because insulin is unavailable to transport sugar into cells for future use. As blood sugar levels rise, the kidneys cannot retain the extra sugar, which is dumped into the urine, thereby increasing urination and causing dehydration. Commonly, about 10% of total body fluids are lost as the patient slips into diabetic ketoacidosis. Significant loss of potassium and other salts in the excessive urination is also common. The most common Continue reading >>

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 >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

INTRODUCTION Diabetic ketoacidosis (DKA) is a very serious complication of diabetes mellitus, a metabolic disorder that is characterized by hyperglycemia, metabolic acidosis, and increased body ketone concentrations. The most common causes of DKA are infection and poor compliance with medication regimens. Other causes include undiagnosed diabetes, alcohol abuse, and a multitude of medical conditions such as cerebrovascular accident (CVA), complicated pregnancy, myocardial infarction, pancreatitis, and stress. Diabetic ketoacidosis is a complicated pathology. Early recognition of DKA, a good understanding of the pathological processes of DKA, and aggressive treatment are the keys to successful treatment. With good care, DKA can be managed and the patient will survive. OBJECTIVES When the student has finished studying this module, he/she will be able to: 1. Identify the correct definition of DKA. 2. Identify a basic function of insulin. 3. Identify the insulin derangements of types I and II diabetes. 4. Identify the basic cause of DKA. 5. Identify two specific causes of DKA. 6. Identify the two pathogenic mechanisms that produce the signs/symptoms of DKA. 7. Identify metabolic consequences of increased hormone concentrations in DKA. 8. Identify the criteria used to diagnose DKA. 9. Identify common signs and symptoms of DKA. 10. Identify laboratory abnormalities seen in DKA. 11. Identify complications of DKA. 12. Identify the three most important therapies for treating DKA. 13. Identify the correct roles of sodium bicarbonate and phosphate in treating DKA. 14. Identify an important rule for using potassium replacement in DKA. 15. Identify an important rule for switching from IV to subcutaneous insulin. EPIDEMIOLOGY Most cases of DKA are seen in patients with type I diabete Continue reading >>

Diabetes With Ketone Bodies In Dogs

Diabetes With Ketone Bodies In Dogs

Studies show that female dogs (particularly non-spayed) are more prone to DKA, as are older canines. Diabetic ketoacidosis is best classified through the presence of ketones that exist in the liver, which are directly correlated to the lack of insulin being produced in the body. This is a very serious complication, requiring immediate veterinary intervention. Although a number of dogs can be affected mildly, the majority are very ill. Some dogs will not recover despite treatment, and concurrent disease has been documented in 70% of canines diagnosed with DKA. Diabetes with ketone bodies is also described in veterinary terms as diabetic ketoacidosis or DKA. It is a severe complication of diabetes mellitus. Excess ketone bodies result in acidosis and electrolyte abnormalities, which can lead to a crisis situation for your dog. If left in an untreated state, this condition can and will be fatal. Some dogs who are suffering from diabetic ketoacidosis may present as systemically well. Others will show severe illness. Symptoms may be seen as listed below: Change in appetite (either increase or decrease) Increased thirst Frequent urination Vomiting Abdominal pain Mental dullness Coughing Fatigue or weakness Weight loss Sometimes sweet smelling breath is evident Slow, deep respiration. There may also be other symptoms present that accompany diseases that can trigger DKA, such as hypothyroidism or Cushing’s disease. While some dogs may live fairly normal lives with this condition before it is diagnosed, most canines who become sick will do so within a week of the start of the illness. There are four influences that can bring on DKA: Fasting Insulin deficiency as a result of unknown and untreated diabetes, or insulin deficiency due to an underlying disease that in turn exacerba Continue reading >>

Diabetic Ketoacidosis And Hyperglycemic Hyperosmolar Syndrome

Diabetic Ketoacidosis And Hyperglycemic Hyperosmolar Syndrome

In Brief Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic syndrome (HHS) are two acute complications of diabetes that can result in increased morbidity and mortality if not efficiently and effectively treated. Mortality rates are 2–5% for DKA and 15% for HHS, and mortality is usually a consequence of the underlying precipitating cause(s) rather than a result of the metabolic changes of hyperglycemia. Effective standardized treatment protocols, as well as prompt identification and treatment of the precipitating cause, are important factors affecting outcome. The two most common life-threatening complications of diabetes mellitus include diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar syndrome (HHS). Although there are important differences in their pathogenesis, the basic underlying mechanism for both disorders is a reduction in the net effective concentration of circulating insulin coupled with a concomitant elevation of counterregulatory hormones (glucagon, catecholamines, cortisol, and growth hormone). These hyperglycemic emergencies continue to be important causes of morbidity and mortality among patients with diabetes. DKA is reported to be responsible for more than 100,000 hospital admissions per year in the United States1 and accounts for 4–9% of all hospital discharge summaries among patients with diabetes.1 The incidence of HHS is lower than DKA and accounts for <1% of all primary diabetic admissions.1 Most patients with DKA have type 1 diabetes; however, patients with type 2 diabetes are also at risk during the catabolic stress of acute illness.2 Contrary to popular belief, DKA is more common in adults than in children.1 In community-based studies, more than 40% of African-American patients with DKA were >40 years of age and more than 2 Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

What Is It? Diabetic ketoacidosis is a potentially fatal complication of diabetes that occurs when you have much less insulin than your body needs. This problem causes the blood to become acidic and the body to become dangerously dehydrated. Diabetic ketoacidosis can occur when diabetes is not treated adequately, or it can occur during times of serious sickness. To understand this illness, you need to understand the way your body powers itself with sugar and other fuels. Foods we eat are broken down by the body, and much of what we eat becomes glucose (a type of sugar), which enters the bloodstream. Insulin helps glucose to pass from the bloodstream into body cells, where it is used for energy. Insulin normally is made by the pancreas, but people with type 1 diabetes (insulin-dependent diabetes) don't produce enough insulin and must inject it daily. Your body needs a constant source of energy. When you have plenty of insulin, your body cells can get all the energy they need from glucose. If you don't have enough insulin in your blood, your liver is programmed to manufacture emergency fuels. These fuels, made from fat, are called ketones (or keto acids). In a pinch, ketones can give you energy. However, if your body stays dependent on ketones for energy for too long, you soon will become ill. Ketones are acidic chemicals that are toxic at high concentrations. In diabetic ketoacidosis, ketones build up in the blood, seriously altering the normal chemistry of the blood and interfering with the function of multiple organs. They make the blood acidic, which causes vomiting and abdominal pain. If the acid level of the blood becomes extreme, ketoacidosis can cause falling blood pressure, coma and death. Ketoacidosis is always accompanied by dehydration, which is caused by high Continue reading >>

Diabetic Ketoacidosis (dka): Treatment Guidelines

Diabetic Ketoacidosis (dka): Treatment Guidelines

Diabetic ketoacidosis (DKA), resulting from severe insulin deficiency, accounts for most hospitalization and is the most common cause of death, mostly due to cerebral edema, in pediatric diabetes. This article provides guidelines on management to restore perfusion, stop ongoing ketogenesis, correct electrolyte losses, and avoid hypokalemia and hypoglycemia and the circumstances that may contribute, in some instances, to cerebral edema (overhydration, rapid osmolar shifts, hypoxia). These guidelines emphasize the importance of monitoring glycemia, electrolytes, hydration, vital signs, and neurologic status in a setting where response can be rapid if necessary (e.g., mannitol for cerebral edema). Most important is the prevention of DKA in established patients by close supervision of those most likely to omit insulin, or during illness, and a high index of suspicion for diabetes to prevent deterioration to DKA in new patients, particularly those under age 5, who are at greatest risk of complications. Continue reading >>

Paediatric Diabetic Ketoacidosis

Paediatric Diabetic Ketoacidosis

Specialist Registrar in Paediatric Intensive Care Continuing Education in Anaesthesia Critical Care & Pain, Volume 9, Issue 6, 1 December 2009, Pages 194199, Simon Steel, Shane M. Tibby; Paediatric diabetic ketoacidosis, Continuing Education in Anaesthesia Critical Care & Pain, Volume 9, Issue 6, 1 December 2009, Pages 194199, Diabetic ketoacidosis (DKA) is the leading cause of morbidity and mortality in children with diabetes. Cerebral oedema is the most common cause of death and a high index of suspicion is always required. Cerebral oedema may be exacerbated by factors related to both DKA presentation and therapy. I.V. fluid boluses should be given cautiously. Always use low-dose insulin regimes and avoid insulin boluses. Misinterpretation of acidbase abnormalities is avoided when changes in pH and base deficit are viewed in conjunction with the anion gap (the latter being a better representation of resolution of ketoacidosis). Diabetic ketoacidosis (DKA) can occur with both types 1 and 2 diabetes mellitus, 1 and is the leading cause of morbidity and mortality in children with diabetes. 2 Unlike the adult population, paediatric mortality is mainly due to the development of cerebral oedema. 1 This article will review the pathophysiology and complications of paediatric DKA and discuss the principles behind current treatment strategies. The incidence of DKA is generally higher for type 1 diabetes, both at presentation and in the setting of established disease. Studies from Europe and the USA have estimated an incidence of DKA at first diabetic presentation of 1570% for type 1 diabetes (with patients under 5 yr of age being at highest risk), and 525% for type 2. 1 , 3 It is thought that the wide variation in incidence within both sub-types is influenced by the availabili Continue reading >>

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