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Dka Case Presentation Ppt

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 >>

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 >>

Episode 63 – Pediatric Dka

Episode 63 – Pediatric Dka

Pediatric DKA was identified as one of key diagnoses that we need to get better at managing in a massive national needs assessment conducted by the fine folks at TREKK – Translating Emergency Knowledge for Kids – one of EM Cases’ partners who’s mission is to improve the care of children in non-pediatric emergency departments across the country. You might be wondering – why was DKA singled out in this needs assessment? It turns out that kids who present to the ED in DKA without a known history of diabetes, can sometimes be tricky to diagnose, as they often present with vague symptoms. When a child does have a known history of diabetes, and the diagnosis of DKA is obvious, the challenge turns to managing severe, life-threatening DKA, so that we avoid the many potential complications of the DKA itself as well as the complications of treatment – cerebral edema being the big bad one. The approach to these patients has evolved over the years, even since I started practicing, from bolusing insulin and super aggressive fluid resuscitation to more gentle fluid management and delayed insulin drips, as examples. There are subtleties and controversies in the management of DKA when it comes to fluid management, correcting serum potassium and acidosis, preventing cerebral edema, as well as airway management for the really sick kids. In this episode we‘ll be asking our guest pediatric emergency medicine experts Dr. Sarah Reid, who you may remember from her powerhouse performance on our recent episodes on pediatric fever and sepsis, and Dr. Sarah Curtis, not only a pediatric emergency physician, but a prominent pediatric emergency researcher in Canada, about the key historical and examination pearls to help pick up this sometimes elusive diagnosis, what the value of serum 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 >>

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 >>

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 >>

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 >>

Diabetic Ketoacidosis Clinical Presentation

Diabetic Ketoacidosis Clinical Presentation

History Insidious increased thirst (ie, polydipsia) and urination (ie, polyuria) are the most common early symptoms of diabetic ketoacidosis (DKA). Malaise, generalized weakness, and fatigability also can present as symptoms of DKA. Nausea and vomiting usually occur and may be associated with diffuse abdominal pain, decreased appetite, and anorexia. A history of rapid weight loss is a symptom in patients who are newly diagnosed with type 1 diabetes. Patients may present with a history of failure to comply with insulin therapy or missed insulin injections due to vomiting or psychological reasons. Decreased perspiration is another possible symptom of DKA. Altered consciousness in the form of mild disorientation or confusion can occur. Although frank coma is uncommon, it may occur when the condition is neglected or if dehydration or acidosis is severe. Among the symptoms of DKA associated with possible intercurrent infection are fever, dysuria, coughing, malaise, chills, chest pain, shortness of breath, and arthralgia. Acute chest pain or palpitation may occur in association with myocardial infarction. Painless infarction is not uncommon in patients with diabetes and should always be suspected in elderly patients. A study by Crossen et al indicated that in children with type 1 diabetes, those who have had a recent emergency department visit and have undergone a long period without visiting an endocrinologist are more likely to develop DKA. The study included 5263 pediatric patients with type 1 diabetes. [15] Continue reading >>

Case Presentation

Case Presentation

History of present illness Pat B is a 48 year old Type I diabetic who was transferred from Darlington ER, where she presented with 3 days of nausea, vomiting and intermittent chills. In the ER, she was found to have a blood sugar of 980, pH 6.96, pCO2 11.2, bicarbonate of 2.5. She was placed on an insulin drip and transferred to Meriter Hospital. Review of systems Most of the history is obtained from the patient’s husband as the patient is unable to provide us with any information as she is obtunded. The patient’s blood sugars have recently been in the 400s, despite her taking insulin and other medications as she usually does. She was drinking a lot of water, but did not complain of chest pain, shortness of breath, cough, sputum production, abdominal pain, diarrhea. Past Medical History Diabetes mellitus Type I for 21 years. Hypertension, well controlled. Seizure disorder, no seizures for “many years†on Lamictal Hysterectomy Breast lumpectomy, benign Right lung resection for “lung spots†Social History Pat is married and the mother of 2 grown up children. She works as a registered nurse at a clinic in Darlington, WI. No history of tobacco or alcohol or illicit drug use. Family History Both parents died of cancer of unknown primary. Siblings and children healthy Physical Exam VITAL SIGNS: BP 98/46, HR 113, Temp 91.3, O2 Sat 99 % on RA. GEN APP: Obtunded middle-aged female breathing spontaneously, answers yes or no to questions. HEENT: R pupil reactive 4mm ïƒ 2 mm. L pupil sluggish and minimally reactive. No oral lesions. Tongue dry and cracked. No carotid bruits, JVD, thyromegaly or LAD. LUNGS: CTA bilaterally. HEART: Tachycardia. No gallops, murmurs, rubs, heaves or thrills. ABDOMEN: Hypoactive bowel sounds. Diffuse, mild to moderate 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 >>

Pediatric Critical Care Medicine

Pediatric Critical Care Medicine

* Goals & Objectives Understand the action of insulin on the metabolism of carbohydrates, protein & fat Understand the pathophysiology of IDDM & DKA Understand the management approach to the patient with DKA Appreciate the complications that occur during treatment * Classification Type I (insulin-dependent diabetes mellitus, IDDM) Severe lacking of insulin, dependent on exogenous insulin DKA Onset in childhood ?genetic disposition & is likely auto-immune-mediated Type II (non-insulin-dependent diabetes mellitus, NIDDM) Not insulin dependent, no ketosis Older patient (>40), high incidence of obesity Insulin resistant No genetic disposition Increase incidence due to prevalence of childhood obesity IDDM: Epidemiology 1.9/1000 among school-age children in the US; 12-15 new cases/100,00 Equal male to female African-Americans: occurrence is 20-30% compared to Caucasian-Americans Peaks age 5-7 yrs and adolescence Newly recognized cases: more in autumn & winter Increase incidence in children with congenital rubella syndrome * Type I DM 15-70% of children with Type I DM present in DKA at disease onset 1/350 of type I DM will experience DKA by age 18 yo Risk of DKA increased by: Very young children Lower socioeconomic background No family history of Type I DM DKA: Most frequent cause of death in Type I DM One of the most common reasons for admission to PICU Decreased renal blood flow and glomerular perfusion Stimulates counter regulatory hormone release Dehydration Increased lactic acidosis Accelerated production of glucose and ketoacids Pt’s then have intestinal ileus causing vomiting and abdominal pain, which prevents them from keeping orally hydrated, and contributing to there dehydration * Type I DM: DKA Electrolytes loss Potassium: 3-5 mEq/kg Phosphate: 0.5-1.5 mmol/k Continue reading >>

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 >>

Endocrinology Division

Endocrinology Division

Surviving DKA (as house staff) Matt Bouchonville Endocrinology Division Thursday School ↓ insulin ↑ counterregulatory hormones DKA + = Hyperglycemia Ketosis Acidosis DKA ↓ insulin ↑ glucagon ↑ gluconeogenesis ↓ glucose utilization ↑ lipolysis ↑ ketone bodies ↓ insulin ↑ glucagon ↑ GH ↑ cortisol ↑ catecholamines ↑ lipase Adipocytes ↑ glycerol ↑ FFA gluconeogenesis ketoacids (acetoacetic acid, betahydroxy butyrate) DKA HHS Absolute Insulin Deficiency Relative Insulin Deficiency ↑ Counterregulatory Hormones ↑ Ketoacidosis Absent or minimal ketogenesis DKA on the rise 2009: 140,000 admissions for DKA ~10% of all diabetes-related admissions Discharges (in Thousands) Year DKA: Mortality rates stable DKA: Mortality rates stable Mortality (%) Age group (yrs) 2006 – Overall mortality rate for DKA: 0.41% Mortality: Precipitating event-related DKA-related Hyperglycemia ïƒ osmotic diuresis ïƒ dehydration ïƒ shock Acidosis ïƒ electrolyte imbalance ïƒ arrhythmias ïƒ impaired cardiac contractility ïƒ shock ïƒ vasodilation ïƒ shock Objectives Diagnosis Management Common “Pitfalls†Clinical cases Diagnosis of DKA Physical Exam Tachycardia Postural hypotension Kussmaul respirations Fruity breath Altered sensorium Abdominal tenderness Clinical presentation Polydipsia/polyuria Constitutional symptoms Nausea/vomiting Abdominal pain (40-75%) Altered sensorium Electrolytes and Hydration Serum Total body deficit Total Water, L n/a 5-8 Laboratory Parameters Na, mEq/kg ↓(↑↔) 7-10 Cl, mEq/kg 3-5 K, mEq/kg ↑ (↓↔) 3-5 Phos, mEq/kg 5-7 Mg, mEq/kg 1-2 Ca, mEq/kg 1-2 The Usual Suspects Factors Precipit 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

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 >>

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