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Hyperglycaemic emergencies in Diabetes mellitus

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Hyperglycaemic emergencies in Diabetes mellitus

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Hyperglycaemic emergencies in Diabetes mellitus

  1. 1. PATHOPHYSIOLOGY AND MANAGEMENT OF HYPERGLYCAEMIC EMERGENCIES IN DIABETES MELLITUS Presenter : Dr. Kapil Dhingra
  2. 2. Diabetes Mellitus : An overview • Diabetes mellitus (DM) refers to a group of common metabolic disorders that share the phenotype of hyperglycemia • Factors contributing to hyperglycemia include : 1. reduced insulin secretion, 2. decreased glucose utilization, 3. increased glucose production
  3. 3. Classification of Diabetes • Type 1 diabetes – β-cell destruction • Type 2 diabetes – Progressive insulin secretory defect • Other specific types of diabetes – Genetic defects in β-cell function, insulin action – Diseases of the exocrine pancreas – Drug- or chemical-induced • Gestational diabetes mellitus
  4. 4. Role of Insulin
  5. 5. Hyperglycaemic Emergencies • Diabetic Ketoacidosis (DKA) • Hyperglycaemic Hyperosmolar State (HHS)
  6. 6. Triad of Diabetic Ketoacidosis HYPERGLYCAEMIA DKA KETOSIS ACIDOSIS
  7. 7. Hyperglycaemic Hyperosmolar State (HHS) – Distinguishing characteristics • Hyperglycemia • Hyperosmolarity • Altered sensorium – Patients are typically Type 2 diabetics
  8. 8. Epidemiology DKA HHS • Average of ~ 100,000 hospitalizations/yr • Annual hospital costs exceed $1 billion • Mortality rate 2-5% • Lack of population-based studies • Less than 1% of diabetes-related admissions • Mortality rate ~ 15%
  9. 9. Pathophysiology of DKA
  10. 10. Pathophysiology of HHS Brain Hyperglycemia Hyperosmolality Pancreas Kidney Liver Muscle Impaired insulin secretion Decreased GFR Gluconeogenesis Impaired glucose uptake Impaired thirst
  11. 11. DKA: Precipitating Events 1. Insulin omission /inadequate administration 2. Infection – Pneumonia, UTI 3. Infarction – ACS, Stroke 4. Trauma 5. New diagnosis of Diabetes- often misdiagnosed
  12. 12. DKA: Symptoms Evolves rapidly within a few hours of the precipitating event(s). 1. Nausea/ vomiting 2. Thirst , polyuria 3. Abdominal pain 4. Shortness of breath 5. Full alertness to profound lethargy or coma
  13. 13. DKA: Physical Findings 1. Dry buccal mucosa, sunken eye balls, poor skin turgor 2. Tachycardia 3. Hypotension/Shock 4. Tachypnea/Kussmaul respirations/respiratory distress 5. Abdominal tenderness (may resemble acute pancreatitis or surgical abdomen) 6. Lethargy/obtundation/cerebral edema/possibly coma
  14. 14. HHS: Precipitating Factors 1. Age > 70 years Contributing Factor- debilitating condition (prior stroke or dementia) or social situation that compromises water intake 2. Infection 3. Myocardial infarction 4. Stroke 5. Undiagnosed/untreated Type 2 diabetes 6. Drugs (corticosteroids, thiazides, dobutamine, terbutaline, second generation antipsychotic agents)
  15. 15. HHS: Symptoms • Onset- insidious • Several-week history of polyuria, weight loss, and diminished oral intake • Mental confusion, lethargy, or coma • Focal neurological deficit • Seizure •Notably absent are nausea, vomiting and abdominal pain
  16. 16. HHS: Signs 1. Altered mental status (confusion to coma) 2. Dehydration 3. Hypotension/“Normal” BP in hypertensive patient 4. Tachycardia 5. Fever/Hypothermia
  17. 17. Initial evaluation • History and physical examination should assess 1. Airway patency 2. Cardiovascular/hydration status 3. Mental status 4. Sources of infection • Urgent assessment 1. Finger-stick glucose 2. Urinalysis (glucose, ketones) 3. IV access 4. ECG- arrhythmias, signs of hypo and hyperkalemia
  18. 18. Five I’s in a Hyperglycaemic crisis 1. Infection 2. Infarction 3. infant (pregnancy) 4. indiscretion (including cocaine ingestion) 5. insulin lack (nonadherence or inappropriate dosing).
  19. 19. Initial Laboratory Tests 1. Arterial blood gas 2. Blood glucose and electrolytes (with calculated anion gap) 3. Creatinine and BUN 4. Serum osmolality 5. Serum ketones 6. Complete blood count 7. Blood and urine cultures 8. Urine pregnancy test -women with childbearing potential.
  20. 20. Labs: Glucose • Usually between 250-600mg/dl (DKA) and 600-1200mg/dl (HHS) • Euglycaemic DKA: 1. Nutritional deficiency/starvation 2. Pregnancy
  21. 21. Labs: Anion Gap • Anion Gap= Na – (Cl + HCO3) • Normal <14 mEq/L; DKA >20 mEq/L • Accumulation of β hydroxybutyrate and acetoacetate
  22. 22. Acidosis • Sine qua non of DKA • s/ HCO3 < 10 mEq/L • pH = 6.8-7.3 • Production and accumulation of ketones in serum
  23. 23. Ketosis • Three types of ketones: a) 2 ketoacids ( β hydroxybutyrate and acetoacetate) b) Neutral ketone acetone • Detected in serum and urine • Nitroprusside reaction converts AA to acetone – Theoretically possible to have ketoacidosis from mainly BHB & have a negative test – Can test by adding Hydrogen Peroxide to urine (converts BHB to AA & allows NP reaction)
  24. 24. Labs: Sodium • Variable sodium levels • Direct effect of hyperglycemia leads to hyponatremia (1.6 meq reduction in serum sodium for each 100 mg/dL rise in the serum glucose) • Secondary effect of osmotic diuresis which causes loss of free water→ hypernatremia • Mostly [ 125-135 (DKA), 135-145 (HHS) ]
  25. 25. Labs: Potassium • Overall potassium deficit – Renal loss with osmotic diuresis – ketone excretion (DKA) – GI loss • However, on initial evaluation, K level is usually normal or elevated – Acidosis – Hyperosmolarity – Insulin deficiency • Take great care in monitoring/repleting K
  26. 26. Labs: Others • Phosphate – Usually body depleted, but initial levels may be normal or high • Amylase – May be elevated (DKA), even without pancreatitis. If pancreatitis is suspected , s/lipase should be done. • Elevated WBC • Hypertriglyceridemia and hyperlipoproteinemia
  27. 27. ADA Diagnostic Criteria DKA Mild Moderate Severe HHS Glc (mg/dL) > 250 > 250 > 250 > 600 pH 7.25-7.30 7.00-7.24 < 7.00 > 7.30 HCO3- (mM) 15-18 10-14 < 10 > 18 Urine ketones + + + Small Serum ketones + + + Small Osmolality Varies Varies Varies > 320 Anion gap > 10 > 12 > 12 < 12 Sensorium Alert Drowsy Stupor/Coma Stupor/Coma Kitabchi AE et al. Diabetes Care (2001) 24:131.
  28. 28. Therapeutic goals Treatment involves 5 key components: 1. Fluid resuscitation 2. Insulin and dextrose infusion 3. Electrolyte repletion 4. Monitoring 5. Treating underlying cause
  29. 29. Fluids, fluids, fluids! • Restores circulatory volume • Diminish concentration of catecholamines, glucagon • ↑ urinary glucose loss
  30. 30. Caution! Excessive therapy may result in • ARDS • Cerebral edema • Hyperchloremic acidosis
  31. 31. Fluid replacement • Initial fluid = 0.9% saline – 15ml to 20ml/kg/hr, about 1-1.5L in 1 hour – 500 ml/h for next 2 hours or 1L /h if in shock – 250-500 ml/h according to hydration status • Subsequent change in fluids – 0.45% saline, 250-500ml/hr • START when urine output improves and BP stable – 5% dextrose, 0.45% saline, 150-250ml/hr • START when blood glucose <200 mg/dl (DKA) and <300mg/dl (HHS) • Endpoint – resolution of DKA/HHS
  32. 32. Insulin administration • Withhold insulin therapy until the serum potassium concentration has been determined (s/K >3.3meq/L) • Initial regular insulin – Goal = reduce hourly glucose by 50-70 mg/dl – Bolus = 0.1U/kg IV – IV infusion = 0.1U/kg/hr – Goal not achieved in 1st hr = double the insulin dose
  33. 33. Insulin administration • BS: 200 mg/dl (DKA) or 300 mg/dl (HHS)  IVF – D5, ½ NS  Insulin rate - 0.05 U/kg/hr • Maintenance  blood glucose 150-200 mg/dl (DKA) and 250-300 mg/dl (HHS) • End Point  Resolution of DKA/HHS • It is important to give the first s.c. injection of insulin approximately 2 hours before stopping the i.v. route. (Long-acting insulin + SC short-acting insulin)
  34. 34. Resolution DKA 1. blood glucose is < 200 mg/dl 2. serum bicarbonate is > 18 3. pH is > 7.30 4. anion gap is < 12 HHS 1. osmolarity is < 320 mOsm/kg 2. gradual recovery to mental alertness.
  35. 35. Who saved me: the insulin or the nurse ?
  36. 36. Clinical Formulae • Anion gap – Na - (Cl + HCO3) – Normal 7-9 (ion-specific electrodes), 8-12 (absorption spectroscopy) • Osmolality – 2(Na+K) + glucose/18 + BUN/2.8 – Approximation is 2(Na+K) + glucose/20 + BUN/3 – Normal 290 + 5 mOsm/kg • Corrected sodium – {[(Glc-100)/100]x1.6}+Na+ meas
  37. 37. Potassium Replacement . • Normal or elevated at the time of diagnosis • Goal : s/K= 4 -5mEq/L • Establish adequate renal function (UO = 50 ml/ hr) K < 3.3 mEq/L K=3.3 mEq/L- 5.3 mEq/L K > 5.3mEq/L Withhold insulin 10 mEq of K/hr Do not give K 40mEq of K/hr till K > 3.3 mEq/L 20-30mEq/L of IVF till s/K betn 4-5 mEq/L Check s/K every 2 hrs
  38. 38. Bicarbonate Therapy pH< 6.9 100 mmol sodium bicarbonate in 400 ml sterile water (an isotonic solution) with 20 mEq KCl 200 ml/h for two hours pH= 6.9- 7.0 50 mmol of bicarbonate in 200 ml of sterile water with 10 mEq KCL Infuse over 1 hr pH>7.0 No sodium bicarbonate •Controversial subject •In patients with pH > 7.0, insulin therapy inhibits lipolysis and also corrects ketoacidosis without use of bicarbonate •Adverse effects 1. hypokalemia 2. decreased tissue oxygen uptake 3. cerebral edema 4. delay in the resolution of ketosis Venous pH should be assessed every 2 hours until the pH rises to 7.0; treatment can be repeated every 2 hours if necessary
  39. 39. Phosphate therapy • Phosphate deficiency – Osmotic diuresis → urinary phosphate losses – Insulin therapy → serum phosphate reenters intracellular compartment • RCT have not demonstrated that phosphate replacement is beneficial in DKA • Adverse complications may occur if P < 1.0 mg/dl – Respiratory depression – Skeletal muscle weakness – Hemolytic anemia – Cardiac dysfunction • May be useful to replace 1/3 potassium as K3PO4, reduce chloride load, prevent hyperchloremic acidosis.
  40. 40. Monitoring 1. Don’t expect much sleep 2. Clinical Status 3. Capillary glucose every 1–2 h 4. Electrolytes (especially K+, bicarbonate, phosphate) and anion gap every 4 h for first 24 h. 5. Blood pressure, pulse, respirations, mental status, fluid intake and output every 1–4 h 6. Venous pH q2-4 hrs 7. Ketones? 8. Consider use of flowsheet
  41. 41. Data Flowsheet
  42. 42. Complications • Lactic acidosis – Due to prolonged dehydration, shock, infection and tissue hypoxia – Should be suspected in pt with refractory metabolic acidosis and persistent anion gap • Arterial thrombosis – Stroke, MI, or an ischemic limb • Cerebral edema – Over hydration of free water, excessively rapid correction of hyperglycemia are risk factors • ARDS – Excessive crystalloid infusion – Pulmonary rales, increased AaO2 gradient
  43. 43. DKA Mortality • Mortality primarily due to precipitating illness • Prognosis worse with – Old Age – Coma – Hypotension – Severe comorbidities
  44. 44. DKA HHS Type of DM T1DM>T2DM T2DM>T1DM Ketosis/acidosis Present Absent Age group Any age Typically elderly Onset Rapid Insidious Nausea/vomiting/abdo Present Absent minal pain Mental changes Less common common Focal neurological deficit uncommon common Seizures uncommon common Prerenal Azotemia mild marked Blood Glucose 250-600 800-1200 Fluid deficit 3-5L 8-10L Addition of dextrose S glucose=200mg/dL s/glucose=300mg/dl Bicarbonate therapy needed Not needed Mortality 2-5% 15%
  45. 45. Prevention • Patient education 1. symptoms of DKA 2. precipitating factors 3. management of diabetes during a concurrent illness.
  46. 46. Prevention • During illness or when oral intake is compromised, patients should 1. frequently measure the capillary blood glucose 2. measure urinary ketones when the serum glucose > 16.5 mmol/L (300 mg/dL) 3. drink fluids to maintain hydration 4. continue or increase insulin; and 5. seek medical attention if dehydration, persistent vomiting, or uncontrolled hyperglycemia develop.
  47. 47. Three Take Home Messages 1. DKA &HHS may be life threatening 2. Fluids and Insulin along with frequent monitoring is essential 3. Watch for hypokalemia and cerebral edema 11/13/2014 5:44:25 AM 47
  48. 48. THANK YOU &

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