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Dka Case Presentation Ppt

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Patient professional reference Professional Reference articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use. You may find the Pre-diabetes (Impaired Glucose Tolerance) article more useful, or one of our other health articles. See also the separate Childhood Ketoacidosis article. Diabetic ketoacidosis (DKA) is a medical emergency with a significant morbidity and mortality. It should be diagnosed promptly and managed intensively. DKA is characterised by hyperglycaemia, acidosis and ketonaemia:[1] Ketonaemia (3 mmol/L and over), or significant ketonuria (more than 2+ on standard urine sticks). Blood glucose over 11 mmol/L or known diabetes mellitus (the degree of hyperglycaemia is not a reliable indicator of DKA and the blood glucose may rarely be normal or only slightly elevated in DKA). Bicarbonate below 15 mmol/L and/or venous pH less than 7.3. However, hyperglycaemia may not always be present and low blood ketone levels (<3 mmol/L) do not always exclude DKA.[2] Epidemiology DKA is normally seen in people with type 1 diabetes. Data from the UK National Diabetes Audit show a crude one-year incidence of 3.6% among people with type 1 diabetes. In the UK nearly 4% of people with type 1 diabetes experience DKA each year. About 6% of cases of DKA occur in adults newly presenting with type 1 diabetes. About 8% of episodes occur in hospital patients who did not primarily present with DKA.[2] However, DKA may also occur in people with type 2 diabetes, although people with type 2 diabetes are much more likely to have a hyperosmolar hyperglycaemic state. Ketosis-prone type 2 diabetes tends to be more common in older, overweight, non-white people with type 2 diabetes, and DKA may be their Continue reading >>

25-40% Of Newly Diagnosed Cases Present In Dka

25-40% Of Newly Diagnosed Cases Present In Dka

Case Scenario #1 What is your assessment? DKA exists when: Venous pH < 7.3 Serum bicarbonate < 15 mEq/dL Blood glucose > 300 mg/dL Presence of ketonemia/ketonuria How much fluid would you administer as a bolus? Would you administer bicarbonate? How much insulin would you administer? What IVF would you start? At what rate? * 10 - 20 cc/kg bolus of NS would be adequate. Though the patient is dehydrated (dry lips), his hemodynamics are good, with acceptable vitals and good perfusion. There would be no reason to administer more than 20 cc/kg fluids. While this patient is clearly acidemic, he is NOT in impending cardiovascular collapse and therefore there is no justification for the administration of bicarbonate. In fact, administration of bicarbonate has been associated with the development of cerebral edema. The “true†serum sodium is 143 133 + 0.016[700-100] Insulin is generally started at 0.1 u/kg/hr. Therefore, in this 30 kg patient, an insulin infusion of 3 u/hr of regular insulin should be initiated. IVF of NS should be started at ~ 2400 cc/m2/day, which is approximately 1.5 x maintenance Continue reading >>

Dka: Critical Care Lecture Series

Dka: Critical Care Lecture Series

Results from an absolute or relative deficiency of circulating insulin Absolute deficiency occurs in previously undiagnosed type 1 or when patients on treatment do not take their insulin, purposefully or inadvertently Relative deficiency happens when counter-regulatory hormones increase due to stress:sepsis, trauma, GI illness Increases-- catecholamines, glucagon, cortisol and growth hormone Low insulin with high counter-regulatory hormones causes an accelerated catabolic state Increase glucose production by the liver and the kidney Via glycogenolysis and gluconeogenesis Impaired peripheral glucose utilization resulting in hyperosmolarity and hyperglycemia Increased lipolysis and ketogenesis resulting in metabolic acidosis and ketonemia Hyperglycemia exceeding the renal threshold and hyperketonemia cause the osmotic diuresis, dehydration and obligatory loss of electrolytes Aggravated by vomiting These mechanisms continues to increase the counter-regulatory hormones which worsen the process Without intervention, life threatening metabolic acidosis and dehydration will occur 4 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 >>

Dka: Management And Pitfalls

Dka: Management And Pitfalls

Published by Daniel Wickerham Modified over 4 years ago Presentation on theme: "DKA: Management and Pitfalls" Presentation transcript: Justin Bright, M.D. Emergency Physicians of NW Ohio February 20, 2013 2 Goals For Today Definitions and characteristics of DKA Appropriate workup Treatment modalities Identify pitfalls and complications Discuss difference in adult vs. pediatric population Management of DKA here at Henry Ford 3 What Is DKA? State of insulin deficiency (absolute or relative) causing dehydration, acidosis, and metabolic derangement By blood work Anion gap metabolic acidosis BHOB > 5 mEq/L Blood glucose > 250 mg/dL pH < 7.3 HCO3 < 18 mEq/L 4 The Stats DKA is reason for 50% of diabetic admissions Tends to occur in patients less than 19 yo Type 1 DM > Type 2 DM Death occurs in 2% of presenting patients 5 Causes of DKA? Underlying Infection (40%) Non-compliance with insulin regimen (25%) New onset diabetes (15%) Medical or surgical stress (20%) AMI Sepsis weak and dizzy Syncope Altered mental status 6 What Is Insulin? Anabolic regulatory hormone Released by pancreas (or administered as supplemental medication) in response to elevated blood sugar Causes blood sugar to be utilized for fuel, with excess stored as muscle and fat Inhibits release of glucagon Inhibits gluconeogenesis and glycogenolysis Hepatic gluconeogenesis and glycogenolysis Fatty acid break down ketogenesis Byproducts: ketones (acetone, BHOB, acetoacetate) Excess blood glucose osmotic diuresis BHOB induces vomiting more dehydration Rising acidosis potassium shift and osmotic loss 9 What Does DKA Look Like? Insidious onset Weakness, fatigue, malaise Polydypsia, polyuria Weakness, fatigue, malaise Abdominal pain and vomiting as BOHB increases Altered level of consciousness May present with symptom Continue reading >>

Diabetic Emergencies

Diabetic Emergencies

Introduction Welcome to your tutorial on diabetic emergencies. This tutorial will take around 45 minutes to complete. You will attempt three case studies with real patients presenting with diabetic emergencies - ketoacidosis, HONK, and insulin-induced hypoglycaemia. Please have a pen and paper handy as you will need them for some of the tasks. These will be reviewed in your seminar relating to this topic. This document should be downloaded and printed out to complete the scenario tasks in the tutorial. Either left-click on the link and follow the instructions on how to save the file, or right-click on the link and select "save target" or "save link as". Objectives To be able to take a history from a patient with hyper- or hypoglycaemia, including demonstrating knowledge of some of the possible causes of their presentation. To be able to perform an initial assessment of a patient with hyperglycaemia in terms of clinical and laboratory investigations. To understand the management principles for a patient with DKA or HONK and to understand differences in management associated with the two conditions. To know how to treat a patient with hypoglycaemia in the emergency setting, and to have an awareness of the intermediate management that that patient may require. A 21 year old man arrives in the department by ambulance. He appears very unwell. The ambulance crew provide you a completed patient report form - select the thumbnail to access the form. What is the important information that you need to obtain from this patient's history? Note this down and then continue with the patient's history on the next page. Patient history This is what the patient tells you.... "I was completely well until two days ago, when I started to feel a bit under the weather. I felt a bit hot and fe Continue reading >>

Exam Shows Diffuse Abdominal Tenderness With Guarding.

Exam Shows Diffuse Abdominal Tenderness With Guarding.

A 14 y/o female is brought to the emergency department by her mother after being found unresponsive at home. She had been ill the day before with nausea and vomiting, but was not running a fever. Her parents had kept her home from school that day. When her mother came home at lunchtime to check on her, she was very lethargic and not responding coherently. By the time she arrived at the hospital, she had to be brought in to the ED on a gurney. Initial evaluation showed O2 sat 100% on room air, pulse 126, respirations 30, BP 92/68, temperature 101.2 F. She appears pale, mucous membranes are dry and she only responds to painful stimuli. Exam shows diffuse abdominal tenderness with guarding. Differential diagnosis? What initial treatment would you suggest? What labs would you order? Any xrays or additional studies? CBC WBC 23,500 Hgb 14.2 g/dL Hct 45% Platelets 425,000 BMP Sodium 126 Potassium 5.2 Chloride 87 CO2 <5 BUN 32 Creatinine 1.5 Glucose 1,376 Arterial Blood Gases pH 7.19 Po2 100 mm Hg HCO3 7.5 mmo/L Pco2 20 mm Hg Sao2 98% (room air) Urine Specific gravity 1.015 Ketones 4+ Leukocytes few Glucose 4+ Nitrates 0 RBCs many Diabetic ketoacidosis (DKA) is an acute metabolic complication of diabetes characterized by hyperglycemia, hyperketonemia, and metabolic acidosis. DKA occurs mostly in type 1 diabetics. It causes nausea, vomiting, and abdominal pain and can progress to cerebral edema, coma, and death. DKA is diagnosed by detection of hyperketonemia and anion gap metabolic acidosis in the presence of hyperglycemia. Treatment involves volume expansion, insulin replacement, and prevention of hypokalemia. Symptoms and signs of DKA Nausea & vomiting Abdominal pain--particularly in children Lethargy and somnolence Kussmaul respirations Hypotension Tachycardia Fruity breath Continue reading >>

Reference

Reference

This purpose of this talk is to overview the 2017 American Diabetes Association Standards of Medical Care in Diabetes. These Standards comprise all of the current and key clinical practice recommendations of the American Diabetes Association. [SLIDE] 2 Reference American Diabetes Association. Standards of medical care in diabetes—2014. Diabetes Care 2014;37(suppl 1):S1 A few notes on the Standards of Care: The Association funds development of the Standards of Care and all Association position statements out of its general revenues and does not use industry support for these purposes [CLICK] The slides are organized to correspond with sections within the 2017 Standards of Care. As we go through I’ll make note of where we are within the document. [CLICK] Though not every section in the document is represented, these slides do incorporate the most salient points from the Position Statement As with all Association position statements, the Standards of Care are reviewed and approved by the Association’s Board of Directors, which includes health care professionals, scientists, and lay people. [SLIDE] 3 These Standards of Care are revised annually by the ADA’s multidisciplinary Professional Practice Committee (PPC) [CLICK] For the 2017 revision, PPC members systematically searched Medline for human studies related to each subsection and published since 1 January 2016. [CLICK] Recommendations were revised based on new evidence or, in some cases, to clarify the prior recommendations or match the strength of the word to the strength of the evidence [CLICK] A table linking the changes in the recommendations to new evidence can be reviewed at professional.diabetes.org/SOC (Standards of Care) [CLICK] The Association and the Professional Practice Committee Continue reading >>

Diabetic Ketoacidosis And Pediatric Stroke

Diabetic Ketoacidosis And Pediatric Stroke

THE CASE: A 6-year-old previously healthy right-handed girl presented with a 3-day history of progressive epigastric abdominal pain, polydipsia and secondary nocturnal enuresis and a 2-week history of weight loss of 5 kg. Her initial assessment revealed tachypnea with Kussmaul's respiration, tachycardia and moderate dehydration, with an estimated fluid deficit of 6%– 9%. The girl was hyperglycemic (plasma glucose level 43.4 mmol/L) and acidotic (pH 7.13, bicarbonate level 3.8 mmol/L), with urinalysis revealing ketonuria and glucosuria. After admission, appropriate fluid resuscitation and insulin treatment were started. The patient's diabetic ketoacidosis resolved over 20 hours, at which point a diabetic diet was introduced along with subcutaneous insulin therapy. On the morning after admission, the patient was found by the nursing staff to be irritable, lethargic and intermittently combative. Twelve hours later a right hemiparesis and aphasia became evident. A cranial CT scan showed an evolving infarct in the left basal ganglia. Transcranial Doppler ultrasonography and magnetic resonance angiography showed occlusion of the proximal left middle cerebral artery (Fig. 1). Echocardiography showed 2 thrombi, measuring 11 х 9 mm and 1 х 1 mm respectively, on the underside of the anterior mitral valve leaflet. There was no associated congenital heart disease. Because of a high risk of further thromboembolic events, heparin infusion was begun, and open thrombectomy was performed on the third day. Pathological examination revealed inflammatory cells and an organized thrombus. Blood cultures and prothrombotic studies yielded negative findings. Intensive rehabilitation therapy and low-molecular-weight heparin (enoxaparin, 30 mg subcutaneously every 12 hours) were started after Continue reading >>

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 >>

Diabetic Ketoacidosis Case Presentation

Diabetic Ketoacidosis Case Presentation

1. DIABETIC KETOACIDOSIS CASE PRESENTATION ICU ,MEDICAL WARD ROTATION 2. Presented by : Walaa Aljuaid , Manal Alosaimi 2. OUTLINES : • THE CASE . • WHAT IS THE DKA • DEFINITION • CAUSES • INCIDENCE AND PREVALENCE • DIAGNOSIS • COMPLICATION • TREATMENT • INTERVENTION 3. THE CASE : ▸ N is a 37 years old female , come to the ER complaining of abdominal pain, shortness of breath, chest pain and palpitation . ER 4. HISTORY OF PRESENT ILLNESS ▸ She has had 2 times Gestational diabetes 4 years ago in her first pregnant and 1 years ago in her second pregnant . ▸ Family history : Unknown ▸ Allergy : No Kind of Allergy . ▸ Medication history : did not mention . ER 5. REVIEW OF SYSTEMS : ‣ Eyes: normal ‣ Mental status: conscious . ‣ Respiratory system: Normal sounds ‣ Cardiovascular system: S1+S2 ‣ Chest wall & breast: No any diseases ‣ Abdomen: soft and lax . ‣ Extremities : No any diseases. ER 6. VITAL SIGN ON ADMISSION ▸ Normal Ranges : ▸ Patient Vital sign : Temperature PR RR O saturation BP 36-37 60-100 16-20 > 96% 120/80 Temperature PR RR O saturation BP 37.3 160 40 98% 130/80 ER 7. LAB TESTS: ▸ Normal Blood Gases : ▸ Patient’s Blood Gases : PH PCO2 PO2 7.35-7.45 32-48 83-108 PH PCO2 PO2 7.002 16.3 63 ER 8. ▸ Glucose ++++ ▸ Ketones +++ URINE ANALYSIS : LAB RESULTS : Glucose mg/dl K Na Cl 70-119 3.5-5.3 135-153 98-110 Normal Ranges Glucose mg/dl K Na Cl 417 4.99 136 99 Patient’s Ranges ER 9. CBC : Normal Ranges WBC 10^9/uL RBC 10^12/uL Hb g/dL 4-10 x10^9/L 4,5 -5,5 X10^12/L 12-16 WBC 10^9/uL RBC 10^12/uL Hb g/dL 12.06 5.5 14 Patient’s Ranges ER 10. FINAL DIAGNOSIS: DIABETIC KETOACIDOSIS 11. WHAT IS THE DIABETIC KETOACIDOSIS ( DKA ) ? ▸ DKA is a life-threatening condition that develops when cells in the body are un 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 >>

Case Presentation

Case Presentation

EM Registrar Case 12 year old male 1/12 fatigue Severe LOW 3/7 increasing SOB 1/7 confusion + lethargy Case Med Hx: Nil Chronic Medication: Nil Allergies: Nil known Multiple GP visits: fatigue due to puberty Case Clinically: Emaciated P 140 BP 70/40 RR 45 Temp 37.6°C Glucose: 36 mmol/l Acidotic breathing, shocked CNS – drowsy, but rousable, orientated to person, not place or time Other systems essentially normal Case Urine Ketones + UEC 129/ 5,2/ 9.3/ 108 ABG pH 7.05 pCO2 1.8 pO2 18 Bicarb 5.2 BE – 20 Case Problems New Type I DM DKA Hypovolaemic Shock Hyponatraemia Cerebral Oedema Management First bolus: 10ml/kg N/Saline – remained hypotensive Second bolus 10ml/kg N/Saline: still hypotensive, but ↑ confusion Concern about worsening cerebral oedema Fluid boluses stopped, commenced on fluid rehydration 0.45% Saline Admitted to ICU CT Brain: cerebral oedema Worsened over next 48 hrs, but eventually made complete recovery Case Type of fluid? Volume for resuscitation? Management of cerebral oedema in DKA? Predictors of cerebral oedema in DKA? Type of Fluid Normal (0.9%) Saline Generally recommended fluid1 Concerns about hyperchloraemic acidosis2 Ringers Lactate3 More hypotonic → increased risk cerebral oedema Lactate potentially metabolised to glucose Non-metabolised lactate can ↓ level of consciousness Contains potassium No evidence to support other crystalloids/ colloids for resuscitation Very little evidence overall for different fluids Best evidence for 0.9% Saline4 If not available, isotonic fluid Consider 0.45% saline for rehydration if hypernatraemic Volume for Resuscitation ≤ 10ml/kg boluses repeat to max 3 doses (30ml/kg)1,5 Fluid bolus not required if not shocked Fluid deficit replacement over 24-48 hrs Lower fluid 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 Emergencies, Part 5: Dka Case Studies

Diabetic Emergencies, Part 5: Dka Case Studies

Case Study 1 A 32-year-old male with type 1 diabetes since the age of 14 years was taken to the emergency room because of drowsiness, fever, cough, diffuse abdominal pain, and vomiting. Fever and cough started 2 days ago and the patient could not eat or drink water. He has been treated with an intensive insulin regimen (insulin glargine 24 IU at bedtime and a rapid-acting insulin analog before each meal). On examination he was tachypneic, his temperature was 39° C (102.2° F), pulse rate 104 beats per minute, respiratory rate 24 breaths per minute, supine blood pressure 100/70 mmHg; he also had dry mucous membranes, poor skin turgor, and rales in the right lower chest. He was slightly confused. Rapid hematology and biochemical tests showed hematocrit 48%, hemoglobin 14.3 g/dl (143 g/L), white blood cell count 18,000/ μ l, glucose 450 mg/dl (25.0 mmol/L), urea 60 mg/dl (10.2 mmol/L), creatinine 1.4 mg/dl (123.7 μ mol/L), Na+ 152 mEq/L, K+ 5.3 mEq/L, PO4 3−2.3 mEq/L (0.74 mmol/L), and Cl− 110 mmol/L. Arterial pH was 6.9, PO 2 95 mmHg, PCO 2 28 mmHg, HCO 3−9 mEq/L, and O 2 sat 98%. The result of the strip for ketone bodies in urine was strongly positive and the concentration of β-OHB in serum was 3.5 mmol/L. Urinalysis showed glucose 800 mg/dl and specific gravity 1030. What is your diagnosis? The patient has hyperglycemia, ketosis, and metabolic acidosis. Therefore, he has DKA. In addition, because of the pre-existing fever, cough, localized rales on auscultation and high white blood cell count, a respiratory tract infection should be considered. The patient is also dehydrated and has impaired renal function. Do you need more tests to confirm the diagnosis? Determination of the effective serum osmolality and anion gap should be performed in all patients presenti Continue reading >>

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