Diabetic emergencies

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  • The universal symbol for diabetes.The purpose of the diabetes symbol is to give diabetes a common identity.Until 2006, there was no global symbol for diabetes. It aims to:support all existing efforts to raise awareness about diabetesinspire new activities, bring diabetes to the attention of the general publicbrand diabetesprovide a means to show support for the fight against diabetes
  • Insulin doses are excessive, ill-timed, or of the wrong type influx of exogenous glucose (overnight fast or following missed meals or snacks)↑ insulin-independent glucose utilization (e.g., during exercise)↑ sensitivity to insulin (e.g., with improved glycemic control, in the middle of the night, late after exercise, or with increased fitness or weight loss)  endogenous glucose production (e.g., following alcohol ingestion) insulin clearance (e.g., in renal failure).
  • Infections – pneumonia, UTI, sepsis, gastroenteritis etc.Inadequate insulin treatment or non-complianceNew onset diabetesInfarction - Myocardial infarction, cerebral, mesenteric, peripheralDrugs – cocaine, atypical antipsychotics, corticosteroids, glucagon, interferon etc.,Pregnancy
  • The anion gap is elevated ([Na + K] - [Cl + HCO3] >13 mEq/L).Plasma osmolarity usually is increased (>290 mOsm/L). If plasma osmolarity cannot be directly measured, it may be calculated as followsPlasma osmolarity = 2 (Na + K) + BUN/3 + glucose/18.
  • Diabetic emergencies

    1. 1. DiabeticEmergencies
    2. 2. ObjectivesGeneral Objective:• Identify the common diabetic complications in an emergency setting.Specific Objective:• Describe diabetic ketoacidosis, hyperosmolar syndrome, and hypoglycemia.• Describe their diagnosis, treatment, and prevention.
    3. 3. Introduction• People with diabetes suffer from diabetic complications that may arise due to erratic blood sugar levels, missed meals, accidental overdose of medications, or too much strenuous exercise. These things could affect the sensitive body of a person with diabetes and could lead to serious incidences of hypoglycemia or hyperglycemia.
    4. 4. Introduction• Uncontrolled blood sugar often contributes to the incidence of diabetic emergencies and complications. Individuals who experience blood sugar levels that are too high or low for prolonged periods of time may develop conditions that could lead to a coma.• Hypoglycemia results from excessively low blood sugar levels caused by either insufficient food consumption or the presence of too much insulin.
    5. 5. Introduction• Diabetic ketoacidosis is a condition that occurs due to an absence or insufficient supply of insulin, which forces the body to burn fat and creates ketones that subsequently accumulate in the body.• Hyperosmolar syndrome is a diabetic condition that results from excessively high blood sugar levels, which cause the blood to adopt a thick consistency.
    6. 6. Hypoglycemia
    7. 7. • Hypoglycemia or low blood glucose is a clinical state associated with <55mg/dl or low plasma glucose with typical symptoms. The Journal of Clinical Endocrinology & Metabolism March 1, 2009 vol. 94 no. 3 709-
    8. 8. Whipples triad Symptoms consistent with hypoglycemia Low plasma glucose concentration Relief of those symptoms after the plasma glucose level is raised The Journal of Clinical Endocrinology & Metabolism March 1, 2009 vol. 94 no. 3 709-
    9. 9. Physiological responses The Journal of Clinical Endocrinology & Metabolism March
    10. 10. Risk factors insulin doses are excessive, ill-timed, or of the wrong type influx of exogenous glucose  insulin-independent glucose utilization  sensitivity to insulin  endogenous glucose production  insulin clearance  The Journal of Clinical Endocrinology & Metabolism March 1, 2009 vol. 94 no. 3 709-
    11. 11. Clinical featuresMILD HYPOGLYCEMIA- mainly adrenergic or cholinergic symptoms Pallor Diaphoresis Tachycardia Palpitations Hunger Paresthesias The Journal of Clinical Endocrinology & Metabolism March 1, 2009 vol. 94 no. 3 709-
    12. 12. Clinical featuresMODERATE HYPOGLYCEMIA (<40 mg/dL)- mainly neuroglycopenic symptoms Inability to concentrate  Confusion Slurred speech  Irrational behaviour Slower reaction time  Blurred vision Somnolence  Extreme fatigue The Journal of Clinical Endocrinology & Metabolism March 1, 2009 vol. 94 no. 3 709-
    13. 13. Clinical featuresSEVERE HYPOGLYCEMIA (<20 mg/dL ) Associated with severe impairment of neurologic function Completely disoriented behavior LOC Coma Seizures The Journal of Clinical Endocrinology & Metabolism March 1, 2009 vol. 94 no. 3 709-
    14. 14. TreatmentMILD HYPOGLYCEMIA Oral carbohydrates (at least 15gm) Sources include • Three glucose tablets (5g each) • 2 ½ cups of fruit juice • ½ to ¾ cup regular soda • 1 cup of milk If patient is unable to take orallyThe Journal of Clinical give IV dextrose Endocrinology & Metabolism March 1, 2009 vol. 94 no. 3 709-
    15. 15. TreatmentMODERATE TO SEVERE HYPOGLYCEMIA Dextrose - 50mL of 50% dextrose IV bolus after blood draw followed by 10% dextrose Glucagon – 1mg IM or SC can be given Effective in treating hypoglycemia only if sufficient liver glycogen present These measures raise blood glucose only transiently Patient is urged to eat as soon as possible The Journal of Clinical Endocrinology & Metabolism March 1, 2009 vol. 94 no. 3 709-
    16. 16. Prevention Patient education Knowing signs and symptoms of hypoglycemia Take meals on a regular schedule Carry a source of carbohydrate Self monitoring of blood glucose Take regular insulin at least 30 min before eating The Journal of Clinical Endocrinology & Metabolism March 1, 2009 vol. 94 no. 3 709-
    17. 17. Diabetic Ketoacidosis
    18. 18.  Acute, major, life-threatening complication of diabetes Increase in the serum concentration of ketones Blood glucose level of greater than 250 mg/dL Blood pH of less than 7.2 Bicarbonate level of 18 mEq/L or less Joint British Diabetes Society guideline for the management of diabetic ketoacidosis Diabetic Medicine Volume 28, Issue 5, pages 508–515, May
    19. 19.  Incidence about 1 out of 2000 Usually occurs in younger individuals but can occur in patients with diabetes at any age Mortality rates are around 2-5% No sex predilection Joint British Diabetes Society guideline for the management of diabetic ketoacidosis Diabetic Medicine Volume 28, Issue 5, pages 508–515, May
    20. 20. Mechanism Absolute or relative insulin deficiency Increased gluconeogenesis Elevation of counter regulatory hormones such as glucagon, cortisol, growth hormone, and catecholamines Joint British Diabetes Society guideline for the management of diabetic ketoacidosis Diabetic Medicine Volume 28, Issue 5, pages 508–515, May
    21. 21. Causes• Infections• Inadequate insulin treatment or non-compliance• New onset diabetes• Infarction• Drugs• Pregnancy Joint British Diabetes Society guideline for the management of diabetic ketoacidosis Diabetic Medicine Volume 28, Issue 5, pages 508–515, May
    22. 22. Classification Moderate Mild DKA Severe DKA DKAPlasma glucose > 250 mg/dl > 250 mg/dl > 250 mg/dlArterial ph 7.25-7.30 7.0-7.24 < 7.0Serum 15-18 10-<15 < 10bicarbonateUrine ketones + + +Anion gap >10 >12 >12Alteration in Joint British Diabetes Society guideline for the alert Alert/drowsy stupor/comasensorium management of diabetic ketoacidosis Diabetic Medicine Volume 28, Issue 5, pages 508–515, May
    23. 23. Clinical presentations• Nausea/vomiting  Thirst/polyuria• Abdominal pain  Shortness of breath• Generalized weakness  Malaise/lethargy• Confusional state• Fever, dysuria, coughing• Chest pain• Palpitations Joint British Diabetes Society guideline for the management of diabetic ketoacidosis Diabetic Medicine Volume 28, Issue 5, pages 508–515, May
    24. 24. Physical findings Tachycardia Signs of dehydration - weak and rapid pulse, dry tongue and skin, hypotension, and increased capillary refill time Tachypnea/ respiratory distress Acetone odor in breath Abdominal tenderness Lethargy/ obtundation/ cerebral edema/ possibly coma Joint British Diabetes Society guideline for the management of diabetic ketoacidosis Diabetic Fever/ Hypothermia 28, Issue 5, pages 508–515, May Medicine Volume
    25. 25. Laboratory findings Hyperglycemia >250mg/dL Serum ketones + ABG:  metabolic acidosis  low bicarbonate  low pH (<7.2) Joint British Diabetes Society guideline for the management of diabetic ketoacidosis Diabetic Medicine Volume 28, Issue 5, pages 508–515, May
    26. 26. Serum electrolytes• Serum potassium may be mildly elevated despite total body potassium deficit• The serum sodium level usually is low (1.6meq reduction in serum sodium for each 5.6mmol/L or 100mg/dL of rise in serum glucose)• The serum chloride and phosphorus levels are low The anion gap is elevated Plasma osmolarity usually is increased (>290 mOsm/L).Joint British Diabetes Society guideline for the management of diabetic ketoacidosis Diabetic Medicine Volume 28, Issue 5, pages 508–515, May
    27. 27. Others Leukocytosis (even without infection) BUN and creatinine are frequently increased Hypertriglyceridemia/ Hyperlipoproteinemia Serum assays for β hydroxybutrate more accurately reflects the true ketone body level• ECG – for detection of hypokalemia/ hyperkalemia, myocardial infarction (silent MI in diabetics) Joint British Diabetes Society guideline for the management of diabetic ketoacidosis Diabetic Medicine Volume 28, Issue 5, pages 508–515, May
    28. 28. Differential diagnosisLACTIC ACIDOSIS most common cause of metabolic acidosis in hospitalized patients presentation is identical to DKA serum glucose and ketones should be normal serum lactate concentration should be greater than 5mm therapy is directed at the underlying cause and optimizing tissue perfusion Society guideline for the Joint British Diabetes management of diabetic ketoacidosis Diabetic Medicine Volume 28, Issue 5, pages 508–515, May
    29. 29. Differential diagnosisSTARVATION KETOSIS due to inadequate carbohydrate availability, resulting in lipolysis and ketone production blood glucose is usually normal blood rarely does have large amounts of ketones arterial pH is normal anion gap is at most mildly elevated Joint British Diabetes Society guideline for the management of diabetic ketoacidosis Diabetic Medicine Volume 28, Issue 5, pages 508–515, May
    30. 30. Differential diagnosisALCOHOLIC KETOACIDOSIS• anion gap is elevated• serum and urine ketones are present• alcoholic ketoacidosis produces an even higher ratio of β-hydroxybutyrate to acetoacetate than DKA does• usually, patient is normoglycemic or hypoglycemic Joint British Diabetes Society guideline for the management of diabetic ketoacidosis Diabetic Medicine Volume 28, Issue 5, pages 508–515, May
    31. 31. Differential diagnosisUREMIC ACIDOSIS Extremely large elevations in the BUN (>200 mg/dL) and creatinine (>10 mg/dL) with normoglycemia pH and anion gap are usually only mildly abnormal treatment is supportive, with careful attention to fluid and electrolytes until dialysis can be performed Joint British Diabetes Society guideline for the management of diabetic ketoacidosis Diabetic Medicine Volume 28, Issue 5, pages 508–515, May
    32. 32. TreatmentIV FLUIDS• 2-3L of 0.9% saline over first 1–3 h (10–15mL/kg per hour)• 0.45% saline at 150-300mL/h (if hemodynamically stable and urine output is adequate )• change to 5% glucose and 0.45% saline at 100–200 mL/h when plasma glucose reaches 250mg/dL (14mmol/L). Joint British Diabetes Society guideline for the management of diabetic ketoacidosis Diabetic Medicine Volume 28, Issue 5, pages 508–515, May
    33. 33. TreatmentINSULIN• if serum K+ is <3.3mmol/L, do not administer insulin until it is corrected to >3.3mmol/L• bolus of IV (0.1 units/kg) or IM (0.3 units/kg) short- acting insulin followed by 0.1 units/kg/hr by continuous IV infusion• Increase 2- to 3-fold if no response by 2–4h Joint British Diabetes Society guideline for the management of diabetic ketoacidosis Diabetic Medicine Volume 28, Issue 5, pages 508–515, May
    34. 34. TreatmentINSULIN• IV regular insulin should be given until the acidosis resolves and the patient is metabolically stable• Intermediate or long-acting insulin, in combination with SC short-acting insulin, should be administered as soon as the patient resumes eating Joint British Diabetes Society guideline for the management of diabetic ketoacidosis Diabetic Medicine Volume 28, Issue 5, pages 508–515, May
    35. 35. TreatmentMONITOR Blood glucose every 1–2 h; Serum electrolytes and anion gap every 4 h for first 24 h. Blood pressure, pulse, respirations, mental status, fluid intake and output every 1–4 h. Joint British Diabetes Society guideline for the management of diabetic ketoacidosis Diabetic Medicine Volume 28, Issue 5, pages 508–515, May
    36. 36. HyperosmolarHyperglycemic State
    37. 37.  The condition is characterized by • Hyperglycemia • Hyperosmolarity • Dehydration without significant ketoacidosis 10.2337/diacare.27.2007.S94 Diabetes Care January 2004vol. 27 no. suppl 1 s94- s102
    38. 38.  Incidence is 1.7 case per 10000 Mortality rate is high (10-20%) and usually due to a co-morbid illness (HHS) has a mean age of onset early in the seventh decade 10.2337/diacare.27.2007.S94 Diabetes Care January 2004vol. 27 no. suppl 1 s94- s102
    39. 39. Pathophysiology Relative insulin deficiency and inadequate fluid intake Insulin deficiency increases hepatic glucose production (through glycogenolysis and gluconeogenesis) and impairs glucose utilization in skeletal muscle Hyperglycemia induces an osmotic diuresis that leads to intravascular volume depletion, which is exacerbated by inadequate fluid replacement 10.2337/diacare.27.2007.S94 Lower levels of counterregulatory hormones and free Diabetes Care January 2004vol. 27 no. suppl 1 s94- fatty acids have been found in HHS than in DKA s102
    40. 40. Clinical featuresHISTORY Usually elderly individual, type 2 DM Mental confusion, lethargy, and coma Absence of nausea, vomiting, abdominal pain Frequent precipitants – pneumonia, sepsis, stroke MI, etc., 10.2337/diacare.27.2007.S94 Diabetes Care January 2004vol. 27 no. suppl 1 s94- s102
    41. 41. vs DKA 10.2337/diacare.27.2007.S94 Diabetes Care January 2004vol. 27 no. suppl 1 s94- s102
    42. 42. TreatmentIV FLUIDS 1–3L of 0.9% normal saline over the first 2–3 h. If the serum sodium >150 meq/L, 0.45% saline should be used. After hemodynamic stability is achieved, the IV fluid administration is directed at reversing the free water deficit using hypotonic fluids (0.45% saline initially then D5W). The calculated free water deficit (which averages 9– 10.2337/diacare.27.2007.S94 10L) should be reversed over the next 1–2 days Diabetes Care January 2004vol. 27 no. suppl 1 s94- (infusion rates of 200–300 mL/h of hypotonic s102
    43. 43. TreatmentINSULIN• IV insulin bolus of 0.1units/kg followed by IV insulin at a constant infusion rate of 0.1units/kg per hour.• If the serum glucose does not fall, increase the insulin infusion rate by twofold• Glucose should be added to IV fluid when the plasma glucose falls to 250 mg/dL, and the insulin infusion rate should be decreased to 0.05– 0.1units/kg per hour. 10.2337/diacare.27.2007.S94 Diabetes Care January 2004vol. 27 no. suppl 1 s94- s102
    44. 44. TreatmentINSULIN The insulin infusion should be continued until the patient has resumed eating and can be transferred to a SC insulin regimen To avoid cerebral edema the blood glucose level should be maintained between 250-300mg/dl until hyperosmolarity and mental status improve and the patient becomes clinically stable 10.2337/diacare.27.2007.S94 Diabetes Care January 2004vol. 27 no. suppl 1 s94- s102
    45. 45. TreatmentPOTASSIUM REPLETION ECG monitoring for hyperkalemia or hypokalemia If K+ < 5.5 give 10-20mEq/hr If K+ < 3.5 give 40-80mEq/hr Administer half as chloride and half as phosphate salts 10.2337/diacare.27.2007.S94 Diabetes Care January 2004vol. 27 no. suppl 1 s94- s102
    46. 46. Monitoring EKG Vital signs 1-2 hourly glucose Serum electrolytes: 2-6 hourly BUN and creatinine: 6-24 hourly Ketones: 6-24 hourly 10.2337/diacare.27.2007.S94 Diabetes Care January 2004vol. 27 no. suppl 1 s94- s102
    47. 47. Pathogenesis of DKA and HHS:stress, infection, or insufficient insulin. FFA, free fatty acid
    48. 48. Conclusion• Diabetic emergencies are common in patients with diabetes, and the effects can be devastating. However, with continued emphasis on the timely and appropriate identification and management of diabetic emergencies, hopefully this may change.• It is therefore important for those with diabetes to keep their sugar levels normal to prevent complications and to be able to live normal, healthy lives.

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