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Diabetic Ketoacidosis Ppt Presentation Free Download

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Presentation on theme: "Diabetic Ketoacidosis"— Presentation transcript: 1 Diabetic Ketoacidosis Dr. Osama Y Kentab, M.D,FAAP,FACEP Assistant Professor of Emergency Medicine - KSAU Clinical Assistant Professor Pediatrics – KSU Consultant Pediatric Emergency Medicine KAMC – KFH - Riyadh 2 Definition 3 Pathophysiology Diabetic ketoacidosis is the result of complex metabolic derangements caused by insulinopenia and increased levels of counter regulatory hormones mainly glucagon. 4 Hyperglycemia glucagon excess (which may be induced both by removal of the normal suppressive effect of insulin and by a concurrent defect in the pancreatic A cell). With hyperglycemia, for example, insulin deficiency impairs peripheral glucose utilization in skeletal muscle and increases both fat and muscle breakdown, leading to enhanced delivery of gluconeogenetic precursors (glycerol and alanine) to the liver . 5 The genesis of ketoacidosis The development of ketoacidosis requires a specific alteration in hepatic metabolism so that free fatty acyl CoA can enter the mitochondria, where conversion to ketones occurs . Mitochondrial entry is regulated by the enzyme carnitine palmitoyl transferase, the activity of which is low in the fed state but is markedly increased by glucagon excess. 6 Hypovolemia 7 Electrolyte Disturbances: Total body potassium is depleted due to renal loss. However , the intial serum potassium is either normal or increase due to acidosis. Once acidosis is corrected the serum level of potassium will decrease. Are always depleted due to renal loss. However, they usually do not present a problem unless they are very low. Phosphate therapy is not recommended because it precipitates with calcium, causing hypocalcemia. 8 Differential diagnosis 9 DIAGNOSIS The diagnosis of DK 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 Ppt Presentation Free Download Management Of Diabetic Ketoacidosis Dka Prof Malhummayyd

Diabetic Ketoacidosis Ppt Presentation Free Download Management Of Diabetic Ketoacidosis Dka Prof Malhummayyd

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Review The Incidence And Pathophysiology Of Dka

Review The Incidence And Pathophysiology Of Dka

Diabetic Ketoacidosis in Children Keystone, July, 2008 Arleta Rewers MD, PhD Robert Slover MD Define the role of patient self-monitoring including blood ketones testing and the healthcare professional advice in preventing DKA Describe current approaches to the clinical diagnosis of DKA, including the role of ketone body levels List treatment options for DKA Definition Hyperglycemia BG > 200 mg/dl (11 mmol/l) (young or partially treated children, pregnant adolescents may present with “euglycemic ketoacidosisâ€) Venous pH <7.3 and/or bicarbonate <15 mmol/L mild DKA pH <7.3 bicarbonate <15 moderate pH <7.2 bicarbonate <10 severe pH <7.1 bicarbonate < 5 Glucosuria and ketonuria/ketonemia (β-HOB) Diabetic Ketoacidosis at Diagnosis of DM in Youth: The SEARCH for Diabetes in Youth Study Incidence of DKA at the time of diagnosis SEARCH is multicenter study In 2002 began population-based ascertainment of incident cases of DM in youth younger than 20 years Incidence: Overall - 25.5% (CI 23.9-27.1) Type 1 - 29.4 % ( CI 27.5-31.3%) Type 2 - 9.7% ( CI 7.1-12.2) Rewers A et al., Pediatrics, May 2008 DKA in children with established T1DM The risk of DKA varies from 1:10 to 1:100 /p-yr Poor metabolic control or previous DKA ï‚ risk Adolescent girls Children with psychiatric disorders, including those with eating disorders Lower socio-economic status Lacking appropriate insurance Inappropriate interruption of insulin pump therapy Predictors of Acute Complications in Children With Type 1 Diabetes A Rewers, HP Chase, T MacKenzie, P Walravens, M Roback M Rewers, RF Hamman, G Klingensmith 2002;287:2511-2518 Cohort of 1,243 diabetic children from BDC - age 0-19 years - residence in the six-county Denver area - outpatient visits between 1/1/1996 - 1/1/2001 Average follow-up 3.2 Continue reading >>

Low-dose Vs Standard-dose Insulin In Pediatric Diabetic Ketoacidosisa Randomized Clinical Trial

Low-dose Vs Standard-dose Insulin In Pediatric Diabetic Ketoacidosisa Randomized Clinical Trial

Importance The standard recommended dose (0.1 U/kg per hour) of insulin in diabetic ketoacidosis (DKA) guidelines is not backed by strong clinical evidence. Physiologic dose-effect studies have found that even lower doses could adequately normalize ketonemia and acidosis. Lowering the insulin dose may be advantageous in the initial hours of therapy when a gradual decrease in glucose, electrolytes, and resultant osmolality is desired. Objective To compare the efficacy and safety of low-dose insulin against the standard dose in children with DKA. Design, Setting, and Participants This was a prospective, open-label randomized clinical trial conducted in the pediatric emergency department and intensive care unit of a tertiary care teaching hospital in northern India from November 1, 2011, through December 31, 2012. A total of 50 consecutive children 12 years or younger with a diagnosis of DKA were randomized to low-dose (n = 25) and standard-dose (n = 25) groups. Interventions Low-dose (0.05 U/kg per hour) vs standard-dose (0.1 U/kg per hour) insulin infusion. Main Outcomes and Measures The primary outcome was the rate of decrease in blood glucose until a level of 250 mg/dL or less is reached (to convert to millimoles per liter, multiply by 0.0555). The secondary outcomes included time to resolution of acidosis, episodes of treatment failures, and incidences of hypokalemia and hypoglycemia. Results The mean (SD) rate of blood glucose decrease until a level of 250 mg/dL or less is reached (45.1 [17.6] vs 52.2 [23.4] mg/dL/h) and the mean (SD) time taken to achieve this target (6.0 [3.3] vs 6.2 [2.2] hours) were similar in the low- and standard-dose groups, respectively. Mean (SD) length of time to achieve resolution of acidosis (low vs standard dose: 16.5 [7.2] vs 17.2 [7.7 Continue reading >>

Acute Complications Of Diabetes - Diabetic Ketoacidosis

Acute Complications Of Diabetes - Diabetic Ketoacidosis

- [Voiceover] Oftentimes we think of diabetes mellitus as a chronic disease that causes serious complications over a long period of time if it's not treated properly. However, the acute complications of diabetes mellitus are often the most serious, and can be potentially even life threatening. Let's discuss one of the acute complications of diabetes, known as diabetic ketoacidosis, or DKA for short, which can occur in individuals with type 1 diabetes. Now recall that type 1 diabetes is an autoimmune disorder. And as such, there's an autoimmune destruction of the beta cells in the pancreas, which prevents the pancreas from producing and secreting insulin. Therefore, there is an absolute insulin deficiency in type 1 diabetes. But what exactly does this mean for the body? To get a better understanding, let's think about insulin requirements as a balancing act with energy needs. Now the goal here is to keep the balance in balance. As the energy requirements of the body go up, insulin is needed to take the glucose out of the blood and store it throughout the body. Normally in individuals without type 1 diabetes, the pancreas is able to produce enough insulin to keep up with any amount of energy requirement. But how does this change is someone has type 1 diabetes? Well since their pancreas cannot produces as much insulin, they have an absolute insulin deficiency. Now for day-to-day activities, this may not actually cause any problems, because the small amount of insulin that is produced is able to compensate and keep the balance in balance. However, over time, as type 1 diabetes worsens, and less insulin is able to be produced, then the balance becomes slightly unequal. And this results in the sub-acute or mild symptoms of type 1 diabetes such as fatigue, because the body isn Continue reading >>

Diabetic Ketoacidosis Ppt Presentation Free Download Diabetic Ketoacidosis Authorstream

Diabetic Ketoacidosis Ppt Presentation Free Download Diabetic Ketoacidosis Authorstream

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Medical Lecture Notes Online

Medical Lecture Notes Online

Anatomy Physiology Biochem Pathology Pharmacology Microbiology forensic Ophthalmology E N T Medicine Gynaecology Obstetrics surgery Paediatrics and many more subject's lecture notes ONLINE. medicalpptonline.blogspot.com contains lecture notes in most fields of medicine. You can directly copy lectures to your laptop ,no need of downloading or streaming Lectures are collected from various sources.I will not be responsible for any typing error and out dated medical facts.Visitors are advised to cross check the information Please give the authors the credit they deserve and do not change the author's name If any of of you have a good personal power point presentations Email me i will upload it here. an acute, life threatening metabolic acidosis complicating IDDM and some cases of NIDDM with intercurrent illness (infection or surgery) usually coupled with an increase in glucagon concentration with two metabolic consequences: 1) Maximal gluconeogenesis with impaired peripheral utilization of glucose 2) activation of the ketogenic process and development of metabolic acidosis. Maximal gluconeogenesis occurs as glucagon lowers the concentration of F2,6-bisphosphate which is the intermediate that activate glycolysis and inhibit gluconeogenesis. This results in hyperglycemia and osmotic diuresis with a resultant dehydration characteristic of DKA. KETOGENESIS occurs as a results of high glucagon/insulin ratio: 1) increased liberation of free fatty acids due to the loss of the inhibitory action of insulin on the hormone sensitive lipase. 2) activation of the transport system (or reestrification to VLDL will occur and nothing will happen) this results in high levels of acetone, acetoacetate and -hydroxybutyrate . anorexia, N/V, along with polydepsia and polyuria for about 24 hrs. f Continue reading >>

Diabetes Care Tasks At School: What Key Personnel Need To Know

Diabetes Care Tasks At School: What Key Personnel Need To Know

* Goal: Optimal Student Health and Learning Ketone Monitoring is a vital piece of a comprehensive plan. * This training component is one of thirteen components created specifically for school nurses and non-medical school personnel who perform diabetes care tasks at school. These components are: • Diabetes Basics • Diabetes Medical Management Plan • Hypoglycemia • Hyperglycemia • Blood Glucose Monitoring • Glucagon Administration • Insulin Basics • Insulin by Syringe and Vial • Insulin by Pen • Insulin by Pump • Ketones • Nutrition and Physical Activity • Legal Considerations This unit is about Ketones. * Learning Objectives Participants will be able to understand: What ketones are Why ketones are monitored When ketones should be monitored When to contact school nurse, parent/guardian, health care provider Participants will be able to demonstrate: How to perform a ketone test * The subject of this unit is ketone monitoring in the school setting. Participants will be able to understand: What ketones are Why ketones are monitored When ketones should be monitored When to contact school nurse, parent/guardian, health care provider Participants will be able to demonstrate: How to perform a ketone test * What Are Ketones? Acids that result when the body does not have enough insulin and uses fats for energy May occur when insulin is not given, during illness or extreme bodily stress, or with dehydration Can cause abdominal pain, nausea, and vomiting Without sufficient insulin ketones continue to build up in the blood and result in diabetic ketoacidosis (DKA) * Ketones are acids that result when the body does not have enough insulin and uses fats for energy. Ketones may be observed when insulin is not Continue reading >>

Diabetic Ketoacidosis

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 Management

Diabetic Ketoacidosis Management

Epidemiology Annual incidence in U.S. 5-8 per 1000 diabetic subjects 2.8% of all diabetic admissions are due to DKA Overall mortality rate ranges from 2-10% Higher is older patients DKA Precipitating Factors Failure to take insulin Failure to increase insulin Illness/Infection Pneumonia MI Stroke Acute stress Trauma Emotional Medical Stress Counterregulatory hormones Oppose insulin Stimulate glucagon release Hypovolmemia Increases glucagon and catecholamines Decreased renal blood flow Decreases glucagon degradation by the kidney Diabetic Ketoacidosis Due to: Severe insulin deficiency Excess counterregulatory hormones Glucagon Epinephrine Cortisol Growth hormone Role of Insulin Required for transport of glucose into Muscle Adipose Liver Inhibits lipolysis Absence of insulin Glucose accumulates in the blood Liver Uses amino acids for gluconeogenesis Converts fatty acids into ketone bodies Acetone, Acetoacetate, β-hydroxybutyrate Increased counterregulatory hormones Increases insulin resistance Activates glycogenolysis and gluconeogenesis Activates lipolysis Inhibits insulin secretion Epinephrine X X X X Glucagon X Cortisol X X Growth Hormone X X X Insulin Deficiency Glucose uptake Proteolysis Lipolysis Amino Acids Glycerol Free Fatty Acids Gluconeogenesis Glycogenolysis Hyperglycemia Ketogenesis Acidosis Osmotic diuresis Dehydration Signs and Symptoms of DKA Polyuria, polydipsia Enuresis Dehydration Tachycardia Orthostasis Abdominal pain Nausea Vomiting Fruity breath Acetone Kussmaul breathing Mental status changes Combative Drunk Coma Atypical Presentations DKA can be present with BS <300 Impaired gluconeogenesis Liver disease Acute alcohol ingestion Prolonged fasting Insulin-independent glucose is high (pregnancy) Chronic poor control but taking insulin Bedside urine Continue reading >>

Canadian Diabetes Association Clinical Practice Guidelines Hyperglycemic Emergencies In Adults

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

Diabetic Ketoacidosis

Diabetic Ketoacidosis (DKA) A state of absolute or relative insulin deficiency aggravated by ensuing hyperglycemia, dehydration, and acidosis-producing derangements in intermediary metabolism, including production of serum acetone. Can occur in both Type I Diabetes and Type II Diabetes In type II diabetics with insulin deficiency/dependence The presenting symptom for ~ 25% of Type I Diabetics. Hyperosmolar Hyperglycemic State (HHS) An acute metabolic complication of diabetes mellitus characterized by impaired mental status and elevated plasma osmolality in a patient with hyperglycemia. Occurs predominately in Type II Diabetics A few reports of cases in type I diabetics. The presenting symptom for 30-40% of Type II diabetics. Diagnostic Criteria for DKA and HHS Mild DKA Moderate DKA Severe DKA HHS Plasma glucose (mg/dL) > 250 > 250 > 250 > 600 Arterial pH 7.25-7.30 7.00-7.24 < 7.00 > 7.30 Sodium Bicarbonate (mEq/L) 15 – 18 10 - <15 < 10 > 15 Urine Ketones Positive Positive Positive Small Serum Ketones Positive Positive Positive Small Serum Osmolality (mOsm/kg) Variable Variable Variable > 320 Anion Gap > 10 > 12 > 12 variable Mental Status Alert Alert/Drowsy Stupor/Coma Stupor/Coma Causes of DKA/HHS Stressful precipitating event that results in increased catecholamines, cortisol, glucagon. Infection (pneumonia, UTI) Alcohol, drugs Stroke Myocardial Infarction Pancreatitis Trauma Medications (steroids, thiazide diuretics) Non-compliance with insulin Diagnostic Studies in DKA/HHS Chemistry ï‚ Glucose  Bicarbonate Anion gap = (Na+) – (Cl- + HCO3-) Frequently seen: ï‚ BUN/creatinine (dehydration) ï‚ potassium  sodium Pseudohyponatremia: to correct, add 1.6 mEq of sodium to every 100mg/dL of glucose above normal Serum acetones Positive in Continue reading >>

Diabetic Ketoacidosis In Type 2 Diabetics: A Novel Presentation Of Pancreatic Adenocarcinoma

Diabetic Ketoacidosis In Type 2 Diabetics: A Novel Presentation Of Pancreatic Adenocarcinoma

Case Description A 75-year-old woman with a 15-year history of type 2 diabetes mellitus, hypertension, hypercholesterolemia, and gastroesophageal reflux disease was admitted with confusion and vomiting. Three days prior to admission, her family noted that she was intermittently confused, had occasional vomiting episodes, and had refused to eat. There was no history of polyuria, polydipsia or diarrhea. For two months prior to admission, she reported a 10–15 pound weight loss, suprapubic discomfort, anorexia and malaise. An upper endoscopy showed changes consistent with Barrett’s esophagus. Colonoscopy and abdominal CT were scheduled but not completed prior to admission. Her diabetes had been well controlled (HbA1c 6–7%) while taking oral hypoglycemic agents (metformin, glipizide and pioglitazone) for several years. One year prior to admission, her primary care physician noted that her blood sugar was elevated despite being adherent to her medications. Insulin (Levemir) was added 6 months later, but adequate glucose control was not achieved. She did not have a history of gallstones or pancreatitis. She was a non-smoker, non-drinker, and she lived alone. She had no family history of diabetes mellitus. On presentation to the emergency room, she was lethargic. Blood pressure was 167/98 mmHg, heart rate 97 beats per minute, respiratory rate 18 breaths per minute and oxygen saturation 97% on room air. She had dry mucous membranes and decreased skin turgor. Breath sounds were present and equal bilaterally, without crackles or wheezes. Heart sounds were normal with a systolic ejection murmur at the left sternal border. Her abdomen was soft and non-distended, with mild suprapubic tenderness, no masses, and normal bowel sounds. On neurological examination, the patient was di Continue reading >>

Ppt Diabetic Ketoacidosis Powerpoint Presentation | Free To Download - Id: 4c140-zdc1z

Ppt Diabetic Ketoacidosis Powerpoint Presentation | Free To Download - Id: 4c140-zdc1z

After you enable Flash, refresh this webpage and the presentation should play. PPT DIABETIC KETOACIDOSIS PowerPoint presentation | free to download - id: 4c140-ZDc1Z The Adobe Flash plugin is needed to view this content The metabolic abnormalities must be corrected in a ... Ileus and gastric atony. State of consciousness. Laboratory 1. Glucose 400-500 mg/dl, but may vary ... PowerPoint PPT presentation Diabetic Ketoacidosis Irene N. Sills, MD Albany Diabetic Ketoacidosis Presentation of new onset abnormalities must be corrected in a careful, Characterized by hyperglycemia and acidosis utilization Osmotic diuresis HYPERKETONEMIA DEHY ion production exceeds utilization ACIDOSIS Chemical buffering by extracellular (bicarbonate) and intracellular buffers (protein, organic and Control of CO2 levels by alveolar ventilation Control of blood bicarbonate concentration by changes in H excretion (excretion of titrable acidity and ammonium) and reabsorption of Hormones that raise glucose catecholamines, Arterial pH less than 7.3 bicarbonate less than 1. Correction of the dehydration (PRIORITY) Immediately decreases levels of anti-insulin Insulin resistance exacerbates the insulin Rehydration will decrease stress hormones Rehydration will improve kidney perfusion DKA is a hypertonic state and should be corrected If clinically in shock, 10-20 cc/kg .9NS or Fluids should be no more hypotonic than .45 NS Maintenance fluid may be .9NS until serum glucose is less than 300 mg/dl when glucose containing Deficit replacement should be given EVENLY over IV infusion rate usually calculates to one and Potassium should be added when patient voids If glucose is lt120-180 mg/dl and acidosis is persisting, it is better to increase the glucose in the infusion rather than decrease the insulin Electr Continue reading >>

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