Management of diabitic_keto_acidosis[1]

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  • GIB=GASTRO6INTESTINAL BLEEDING .CVA=STROKE
  • GH=GROWTH HORMON
  • MA= Metabolic Acidosis
  • HAGMAK= HIGH ANION GAP METABOLIC ACIDOSIS and ( KETONURIA) KETONEMIA / AG=ANION GAP / MA =METABOLIC ACIDOSIS / ABG =ARTERIAL BLOOD GAZES
  • BG=BLOOD GLUCOSE
  • CO=CEREBRAL EDEMA .
  • 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
    12. 12. INVESTIGATIONS • • • • • Urea, creatinine, URINALYSIS for MCS & KETONES PROTEIN,PROTEIN ELECTROLYTES, B/CULTURES CARDIAC ENZYMES (PRN)
    13. 13. MANAGEMENT OF DKA I.ABC evaluation II.TWO LARGE VEINS ACCESES III.Fluid replacement IV.INSULIN V.Potassium VI.BICARBONATE VII.ADDITIONAL PROCEDURES
    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

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