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Management of diabitic_keto_acidosis[1]

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Management of diabitic_keto_acidosis[1]

  1. 1. Management of Diabetic Keto Acidosis
  2. 2. PLAN • • • • • • • • • • Definition Etiology PATHOGENESIS Clinical manifestation Physical examination Differential Diagnosis Laboratory findings MANAGEMENT PROGNOSIS, COMPLICATIONS REFFERENCES
  3. 3. DIFINITION • DKA is an acute life- threatening Sd caused by lack Insulin and, • it represents a derangement of the body`s normal response to starvation, in IDDM(Type 1). • DKA=⇑⇑⇑ glycemia+Ketonemia +Acidosis
  4. 4. ETIOLOGY DKA⇐ Noncompliance with insulin Infection process, Stress, Pregnancy, Trauma, Alcohol abuse in DM-type I, MI, CVA, GIB, New-onset diabetic.
  5. 5. PATHOGENESIS 1.Lack Insulin ⇒ ⇓ Peripheral use of glucose and subsequently ⇒ ⇑⇑⇑blood sugar. ⇒Glucose is unavailable for cellular metabolism 2. Body responses by counter-regulatory hormones(glucagons,cathecolamines,cortisol and GH). Stimulate the production of glucose and ⇒ ⇑⇑⇑blood sugar. 3.In addition, hepatic gluconeogenesis is stimulated ⇒ ⇑⇑⇑blood sugar.
  6. 6. PATHOGENESIS ( CON`T) • Source of energy is needed, thus liver begins to break down free fatty acids i.e. LYPOLYSIS ⇒Ketoacids used by the Brain and other tissues as substrates energy ⇒Ketonemia + Metabolic acidosis. The acidosis ⇒ Intracellular K+ to shift to extra cellular space ⇒ relative Hyperkalemia (despite a total body potassium ⇓ ⇓ ⇓ ⇓).
  7. 7. PATHOGENESIS( CON`T) • Hyperglycemia with Ketonemia ⇒ Hyperosmolar state ⇒osmotic diuresis ⇒ volume depletion, electrolytes loss and the sequela of DKA.
  8. 8. Clinical manifestation • HISTORY is very important !!!!!!! A.Hyperglycemia symptom`s: - Blurred vision - Polyuria - Polydipsia DM= D’se of 3P’s -Polyphagia B.DKA symptoms at beginning: Nausea, Vomiting, abd pain, fruity breath odor. at progress DKA: Dehydration, dizziness, weakness, altered mental status/ shock.
  9. 9. Clinical manifestation(con`t) • Physical Examination= Dehydration(dry mucous membranes, poor skin turgor), hypotension, tachycardia, ± abd tenderness, ± stretching of liver capsule, ± tachypnea or Kusmaul breathing=a rapid, deep,and labored breathing as compensatory response to MA=> Air hunger, smell of acetone
  10. 10. DIFFERENTIAL DIAGNOSIS • HHNKS( hyperosmolar hyperglycemic nonketotic syndrome). • Alcohol ketoacidosis • Sepsis • Gastroenteritis,UTI, Pancreatitis • Uremia • Methanol,ethylene glycol or paraldehyde ingestion • Starvation ketoacidosis • Lactic acidosis
  11. 11. INVESTIGATIONS • DKA= Glucose greater than 250mg /dl = HCO-3 less than 15 meq / l =pH less than 7.3 = ⇑⇑⇑ β hydroxybutyric acid and acetoacetic acid ⇒ HAGMAK = ⇓ Na+ by urinary loss = Total body K+ ⇓ by renal loss, but because of the intracellular shifts of K+ because of the acidosis, K+ serum level is normal or ⇑. ABG ⇒ MA with AG. ECG ⇒ Hyperkalemia / Hypokalemia, MI CXR ⇒ Pneumonia (precipitating factor cause of DKA), Abd. U/S
  14. 14. MANAGEMENT OF DKA 1.ABC evaluation 2.Fluid replacement . N. saline 0.9% (NaCl) 1litre/30 mins 1L / 2 hrs 1l over next 2-4hrs When blood glucose< 15mmoll(250mg/dl) switch to 5% dextrose 1 litre 8- hourly. If dehydration is still +, continue 0.9% saline and add 5%dextrose 1 litre / 12hrs Fluid requirement=6-8 L/24hrs except in elderly people where a fluid overload is avoided. ∆ Fluid requirement should be based on clinical response including urinary output
  15. 15. MANAGEMENT OF DKA 3.INSULIN a. STANDARD PROTOCOL . 50u soluble insulin in 50ml 0.9% saline iv via infusion pump: 6u/hr initially 3u/hr if BG <250mg/dl(12mmoll) 2u / hr if BG<180mg /dl(10mmoll) • Check B/Sugar hourly initially, if no ⇓ Insulin infusion ⇒ ⇑. • Aim= to fall 55-110mg (36mmol / l) / hr
  16. 16. B.If IV INFUSION OF INSULIN IS NOT POSSIBLE 1.A loading dose of 10-20 units of soluble insulin in IM injection, immediately thereafter 5 U/hr. 2. Alternatively, a fast acting insulin 10 -20 u/h in subcutneous injection ( initially 0.3 u/kg body weight, then 0.1u/kg/hr. The concentration of BG should ↓ 55-110mg/hr. If BG does not ↓ after 2 hrs of the commencing TTT, the dose of insulin can be doubled, still a good response is obtained . When BG has follen to 180-270mg/dl, the dose of insulin should be reduced to 1-4 units/hr ,then consider iv Glucose NB: AVOID S/C INSULIN IN Pts WITH LOW BP (SBP<90mmHg).
  17. 17. CONT Restoration of the usual insulin regimen, by SC injection, should not be instituted untill the patient is not able to eat , drink normally.
  18. 18. MANAGEMENT OF DKA 4.Potassium .None in first litre of iv fluid unless < 3.0 mmol / L . If plasma K+ <3.5mmol give 40 mmol added potassium in 1L fluid .Avoid infusion rate> 20mmol / hr .If plasma K+ is 3.5-5.0 mmol, give 20 added K+ . If >5.0mmol/L or anuric patient, no added K+ Avoid K+ within the first 6hrs if no K+ monitoring
  19. 19. 5.BICARBONATE Severely acidotic where pH <7.0 TTT =300ml of 1.26% of NaHCO3- infusion / 30min into elarge vein. ∆ but its use is nowdays contreversial.
  20. 20. 6.ADDITIONAL PROCEDURES IN MGMNT OF D KA . Catheterisation if anuric status in 3hrs .NGT to keep stomach empty if sub / or coma state, vomiting+++ . CV line if CVS is compromised for allowing fluid replacement to be adjusted accuretely . Plasma expander (macromolecular fluid) if SBP<90mmHg or not rise with IV saline . ATB if infection or suspected. . ECG monitoring in severe case . TTT according to the complications.
  21. 21. PROGNOSIS ↑ Mortality = 5 -10% ↑ in elderly ↑ complications
  22. 22. COMPLICATION OF DKA 1 CO due to ↑ blood glucose or use hypertonic fluid and / or Bicarbonate =↑mortality. 2. ARDS. 3. Thromboembolism 4. DIC.(DISSEMINATED INTRAVASC COAG.) 5.ACF. (ACUTE CARDIAC FAILURE) 6.ACUTE GASTRIC DILATATION 7.REBOUND KETO ACIDOSIS _
  23. 23. REFFERENCES • HARRISSON’S 16th edition-2006 • DAVIDSON’s 20th edition-2006 • EMERGENCY MEDICINE 31th edition