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Diabetic Ketoacidosis dr salah mabrouk


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Diabetic Ketoacidosis dr salah mabrouk

  1. 1. Diabetic Ketoacidosis Local seminar Medical Oncology department By Salah Mabruok Khalaf Master internal medicine MD Medical Oncology South Egypt Cancer Institute 2013
  2. 2. Overview• Definition• Epidemiology• Pathophysiology of DKA• Etiology• Clinical manifestation• Investigations• Differential Diagnosis• Prevention• Treatment• Pitfalls in DKA• A guide protocol
  3. 3. DKA Definition DKA = 3 letters= triad of D K A Diabetic glucose >250 mg/dL (usually 500-800) Keto ketones producedketones – both in urine and in serumacetoacetate, acetone, betahydroxybutyratefruity smell, not often encountered in real life)consider that if these criteria aren’t met, it may not be DKA Acidosis Increased anion gap, metabolic acidosis; HCO3- <15, pH<7.30
  4. 4. Epidemiology• Annual incidence in U.S. – 5-8 per 1000 diabetic subjects• 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.• Higher incidence below 5 years• 2.8% of all diabetic admissions are due to DKA• Overall mortality rate ranges from 2-10% – Higher is older patients
  5. 5. Pathophysiology Normal Counterregulatory hormonesInsulin Glucagon, Epinephrine, Cortisol, Growth hormone
  6. 6. Pathophysiology DKAInsulin deficiency Excess counterregulatory hormones
  7. 7. Insulin Deficiency Glucose uptake Lipolysis Proteolysis Glycerol Free Fatty Acids Amino Acids GluconeogenesisHyperglycemia Glycogenolysis KetogenesisOsmotic diuresis Acidosis Dehydration Excess counterregulatory hormones
  8. 8. Etiology• Insulin deficiency • Excess Counterregulatory – Insulin missed dose hormones – Pancreatitis – Infection i.e. Pneumonia – Heavy meal – MI – Stroke – Trauma – Emotional – Pregnancy – Iatrogenic
  9. 9. Clinical manifestations Insulin Deficiency Glucose uptake Lipolysis Proteolysis Glycerol Free Fatty Acids Amino Acids Gluconeogenesis Hyperglycemia Glycogenolysis Ketogenesis Osmotic diuresis Polyuria Electrolyte imbalance Acidosis Polydipsia Fruity breath (acetone smell) Kussmaul breathing (acidotic)Dehydration Mental status changesDry tongue Tachycardia Hypotension Abd pain
  10. 10. Clinical manifestationsSpecial notes• Abdominal pain It is more common in children than in adults It is multifactorial  dehydration of muscle tissue  Delayed gastric emptying  Ileus from electrolyte disturbances  Metabolic acidosis; It sometimes mimicks acute abdomen It is classically periumbilical
  11. 11. Differential Diagnosis• DD of acidotic breathing – Renal failure – Amonia increase in HCF – Hysterical• DD of diabetic coma – Lactic acidosis – Hyperosmolar non-ketotic coma – Hypoglycemia• DD of coma in general• DD of acute abdomen
  12. 12. DKA vs. HHS DKA HHSAge More in children More in elderlyDM type More in type I More in type IIGlucose > 250 > 600Ketonuria/emia +++++ + or -pH <7.3 >7.3HCO3 <15 >15S osmolarity Variable HyperosmolaritySensitivity to insulin Variable Sensitive to small dose
  13. 13. DKA vs. HYPOGLYCEMIA DKA HypoglycemiaEtiology Insulin deficiency or increased Insulin overdose or counter-reg hormones hyperinsulinemiaOnset Gradual AcuteSymptoms and signs S of hyperglycemia -S of Brain glucopenia S of dehydration - S of sympathetic overactivity S of acidosisRBS hyperglycemia hypoglycemiaKetonuria Yes NoKetonemia Yes NoIV glucose No effect Rapidly recover if early Golden rule Any diabetic patient with DKA versus hypoglycemia, give glucose even before glucose measuring
  14. 14. Investigations For diagnosisTriad for diagnosis1. RBS  Hyperglycemia > 300 mg/dl2. Ketonemia and ketonuria3. Blood gas metabolic acidosis – pH < 7.35, anion gap (Na + K) – (Cl + Bicarb) > 10, and Bicarbonate <15 mEq/L
  15. 15. Investigations For diagnosis• Other findings – Electrolyte serum level • Hyperkalemia (rarely Hypokalemia), Hyponatremia (rarely Hypernatremia ) – Investigation for the cause such as • Urine Analysis, AMI panel and ECG, Chest x-ray – Hyperosmolarity • Normal = 285-295 milli-osmoles per kilogram (mOsmol/kg) • [Glucose] and [BUN] are measured in mg/dL
  16. 16. Investigations For Monitoring• RBS – Every 1 hour till RBS reaches 200 mg/dL or less, then every 6 hours• Urine ketones – Every 8h• Blood gas after fluid replacement• Electrolyte serum level every 4 hours till correction
  17. 17. Treatment of DKA• Treatment of predisposing factors• Initial hospital management – Care of comatosed patients – Fluid and electrolytes replacement – Insulin replacement and glucose administration when needed – Treatment of complications• Once resolved – Convert to home insulin regimen – Prevent recurrence
  18. 18. Fluids and Electrolytes• Fluid replacement – Restores perfusion of the tissues – Average fluid deficit 3-6 liters• Initial resuscitation with saline – 1 L of normal saline over the first ½ hour then – ½ L of normal saline over ½ hour then – ½ L of normal saline over 1 hour then – ½ L of normal saline over 2 hours – Then the rate will depend on clinical judge (BP, CVP, basal lung crepitation)
  19. 19. Fluids and Electrolytes• K+ level – If Hyperkalemia (> 5.5 meqlL) • initially present • No treatment as it resolves quickly with insulin drip – If normal level (3.5-5.5 meqlL) • Add 26 mmol for each Liter of infused fluid – If Hypokalemia (<3.5 meqlL) • Add 39 mmol for each Liter of infused fluid
  20. 20. Fluids and Electrolytes• Phosphate deficit – May want to use potassium phosphate• Bicarbonate – Not given unless pH <7 or bicarbonate <5 mmol/L or unresolved acidosis after fluid replacement BW x Becar deficit – Dose (mmol of NaHco3) = ------------------------------------------- 6 BW x Becar deficit – Dose (No of ampoules of NaHco3) = ---------------------------------------- 150
  21. 21. Fluids and Electrolytes• Na level: – Calculate the corrected Sodium (for each 100 mg/dL glucose above 100, add 1.6 meq/l to Na level) • If corrected Na is High or Normal  use Half NS (250-1000 ml/hr) • If corrected Na is Low  use NS, rate depends on severity of volume depletion
  22. 22. Insulin Therapy• Initial dose – IV bolus of 0.1-0.2 units/kg (~ 10 units) regular insulin – Infusion insulin at 0.1 units/kg/hr (max 8 units/hr). • Maintenance dose (Check BG Q1hour, goal is 50-80 mg/dl/hr) – If falling too rapidly, decrease the rate – If falling too slowly increase the rate by 50-100%• Continue IV insulin until urine is free of ketones and RBS reaches 250-300 mg/dl
  23. 23. Insulin Therapy• When RBS reaches 250-300 mg/dl – Decrease the rate of insulin inf to 0.05-0.1 IU/kg/hr (goal is to keep RBS in this range until the gap closes (normal gap 7-8 mEq/l) then start home maintenance SC insulin under umbrella of infused insulin for 2 hours, then continue on SC insulin only .
  24. 24. Glucose Administration• Supplemental glucose – Hypoglycemia occurs • Insulin has restored glucose uptake • Suppressed glucagon – Prevents rapid decline in plasma osmolality • Rapid decrease in insulin could lead to cerebral edema• Glucose decreases before ketone levels decrease• Start glucose when plasma glucose < 300 mg/dl
  25. 25. Insulin-Glucose Infusion for DKABlood glucose Insulin Infusion D5W Infusion <70 0.5 units/hr 150 ml/hr 70-100 1.0 125 101-150 2.0 100 151-200 3.0 100 201-250 4.0 75 251-300 6.0 50 301-350 8.0 0 351-400 10.0 0 401-450 12.0 0 451-500 15.0 0 >500 20.0 0
  26. 26. Complications of DKA• Infection • Pulmonary Edema – Precipitates DKA – Result of aggressive fluid – Leukocytosis can be secondary resuscitation to acidosis • Cerebral Edema• Shock – First 24 hours due to aggressive – If not improving with fluids r/o correction of hypoglycemia or MI administration of hypotonic solution• Vascular thrombosis – c/p: Mental status changes – Severe dehydration – Tx: Mannitol – Cerebral vessels – May require intubation with – Occurs hours to days after DKA hyperventilation
  27. 27. Causes of Cerebral EdemaMechanism:• The brain adapts by producing intracellular osmoles (idiogenic osmoles) which stabilize the brain cells from shrinking while the DKA was developing.• When the hyperosmolarity is rapidly corrected, the extracellular fluids is corrected faster than brain cells – The brain becomes more hypertonic than the extracellular fluids → water flows into the cells → cerebral edema
  28. 28. Causes of Cerebral EdemaThe many factors have been implicated: Rapid and/or sharp decline in serum osmolality with treatment. High initial corrected serum Na concentration. High initial serum glucose concentration. Failure of serum Na to raise as serum glucose falls during treatment. Osmolality Na Glucose
  29. 29. Presentations of Cerebral EdemaCerebral Edema Presentations include: Deterioration of level of consciousness. Headache and blurring of vision Vomiting Convulsion.
  30. 30. Treatment of Cerebral Edema• Reduce IV fluids• Raise foot of Bed• IV Mannitol• Elective Ventilation• Dialysis if associated with fluid overload or renal failure.• Use of IV dexamethasone is not recommended.
  31. 31. Prevention of DKA• Never omit insulin – Cut long acting in half• Prevent dehydration and hypoglycemia• Monitor blood sugars frequently• Monitor for ketosis• Provide supplemental fast acting insulin• Treat underlying triggers• Maintain contact with medical team
  32. 32. Pitfalls in DKA• Plasma glucose is usually high but not always – DKA can be present with RBS < 300 due to • Impaired gluconeogenesis – Liver disease – Acute alcohol ingestion – Prolonged fasting – Insulin-independent glucose is high (pregnancy) • Chronic poor control but taking insulin• Ketone in urine may be –ve in DKA, but always +ve in blood – Due to measurement of acetoacetic acid in urine not, betahydroxybuteric acid – Acetone in blood should be done in this case
  33. 33. Pitfalls in DKA• High WBC may be present without infection• Infection may be present without fever• High Creatinine may be present without true renal function: it may cross react with ketone bodies.• Blood urea may be elevated with prerenal azotemia secondary to dehydration.• Serum amylase is often raised even in the absence of pancreatitis
  34. 34. Email: salahmab76@yahoo.comEmail: Facebook: Dr salah mabrouk Facebook: Dr salah mabrouk YouTube channel: salahmab1 YouTube channel: salahmab1 Mobil: (202) 01004081234 Mobil: (202) 01004081234