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Diabetic Keto acidosis DKA

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  • 1. Diabetic Emergencies-Preventing Secondary Injuries Dr Farhan Shaikh Consultant Pediatric Intensivist Rainbow Children’s Hospital Hyderabad
  • 2. Epidemiology
    • Type1Diabetes accounts for 5% to 10% of the total cases of diabetes worldwide .
    • Type1Diabetes has been historically, and continues to be, the most common type of diabetes in children and adolescents
    • although type 2 diabetes (T2D) is increasingly diagnosed in youth.
    American Diabetes Association. Diabetes Care 2009 Dabelea D et al. Incidence of diabetes in youth in the United States. JAMA 2007
  • 3. Diabetic Emergencies
    • Acute onset
      • DKA
        • Cerebral edema
        • Hypo/Hyperkalemia
        • Venous thrombosis
      • Hypoglycemia
      • HHG
    • Long term
    • Microvascular
      • Retinopathy,
      • Nephropathy and
      • Neuropathy
    • Macrovascular
      • Cardiovascular disease
      • Cerebrovascular accidents
      • Peripheral vascular disease
    Boyle JP, et al. Projection of diabetes burden through 2050: Diabetes Care 2001
  • 4. Diabetic Keto Acidosis
    • Hyperglycemia
    • Blood glucose >11 mmol/L ≈ 200 mg/dL
    • Venous pH <7.3 or Bicarbonate <15 mmol/L
    • Ketonemia and Ketonuria.
    DUNGER DB, et al. Consensus statement on diabetic ketoacidosis in children and adolescents. Arch Dis Child 2004 Feb .
  • 5. Epidemiology DKA
    • 15 -70% of Type 1 Diabetic children can present for the first time as DKA
    • In case of indian children it continues to be the most common initial presentation and has a high mortality
    Geographical variation of presentation at diagnosis : EURODIAB Pediatric Diabetes2009 Wolfsdorf et al. study. European and Dibetes. Diabetologia 2001 Alvi NS et al, DKA in sian children Arch disease Childhood 2001
  • 6. Children in DKA can die from
    • Most Common
    • Cerebral oedema
    • Hypokalemia
    • Aspiration pneumonia
    British society of Pediatric Endocrinology D ept Recommended DKA Guidelines 2009
  • 7. Rare causes of Mortality
    • Hyperkalemia
    • Severe hypophosphatemia
    • Hypoglycemia
    • Sepsis
    • Pulmonary edema, ARDS
    • Rhabdomyolysis
    • Acute renal failure
    • Acute pancreatitis
    EDGE JA et al. Causes of death in children with insulin dependent diabetes 1990-96. Arch Dis Child 1999 .
  • 8. Cerebral Oedema
    • Mortality rate from DKA in children is 0.15% to 0.30%
    • Cerebral edema accounts for 60% to 90% of all DKA deaths
    • From 10% to 25% of survivors of cerebral edema have significant residual morbidity
    LAWRENCE SE et al.Population-based study of incidence and risk factors or cerebral edema in pediatric diabetic ketoacidosis. J Pediatr 2005 May CURTIS JR et al. Recent trends in hospitalization for diabetic ketoacidosis in Ontario children. Diabetes Care2002 Sep.
  • 9. Mechanism of Cerebral Oedema
    • Pathophysiology still remains enigmatic
    • Ideogenic osmotically active substances that regulate cell volume against the osmotic gradient
    • Cerebral hypoperfusion and reperfusion
    • Direct effect of ketone bodies and inflammatory cytokines
    Fuhrman & Zimmerman, Pediatric critical care 4 th edition 2011
  • 10. Factors contributing to development of cerebral oedema
      • More severe acidosis at presentation
      • Increased Blood urea nitrogen at presentation
      • Attenuated rise in measured serum sodium concentrations during therapy
    EDGE J et al. The UK case-control study of cerebral oedema complicating diabetic ketoacidosis in children. Diabetologia 2006
  • 11.
      • 4. Greater volumes of fluid given in the first 4 hour
      • Administration of insulin in the first hour of fluid treatment
      • Bicarbonate treatment for correction of acidosis
    GLASER N et al. Risk factors for cerebral edema in children with diabetic ketoacidosis. N Engl J Med 2001 Jan
  • 12. Preventive Strategies
    • Volume of fluids.
    • Type of fluid
    • Rate of administration
    • Appropriate Change of fluid
    • Close Monitoring
  • 13. Volume of fluid
    • In case of shock give 10 ml/kg 0.9% saline (maximum of 30 ml/kg) slowly over 30 minutes.
    • Requirement = Maintenance + Deficit – fluid already
    • given
    • Deficit (litres) = % dehydration x body weight (kg) (Ensure this result is then converted to ml)
    • For most children, use 5% to 8% dehydration to calculate fluids
    • Earlier assumptions of 10% dehydration are no longer used
  • 14. Maintenance requirement
    • Using Holiday Segar formula for calculation of maintainence IV fluids results in excess fluid administration
    • 0 – 12.9 kg 80 ml/kg/24 hrs
    • 13 – 19.9 kg 65 ml/kg/24 hrs
    • 20 – 34.9 kg 55 ml/kg/24 hrs
    • 35 – 59.9 kg 45 ml/kg/24 hrs
    • (>60 kg) 35 ml/kg/24 hrs
    British Society of Pediatric and Endocrinology Recommended DKA Guidelines 2009
  • 15. Calculation
    • Hourly rate = 48 hr maintenance + deficit – resuscitation fluid
    • 48
    • In a 20 kg 6 year old boy who is 8% dehydrated, and who has already had 20ml/kg saline, will require
    • Deficit ( 8 % x 20 kg) = 1600 mls
    • Maintenanace (55ml x 20kg ) = 1100 mls each 24 hours
    • 48 hr Maint + deficit = 1100+1100+1600 = 3800 mls
    • Resucitation fluid (20kg x 20ml ) = 400 mls
    • Final amount = 3800 – 400 = 3400
    • Hourly rate over 48 hrs = 3400 mls = 71 mls/hour
    • Do not include continuing urinary losses in the calculations at this stage
  • 16. Bottom line..
    • Whatever may be your final calculation, make sure that total fluid administered in each day (24hrs)does not exceed 1.5–2 times the usual daily maintenance requirement based on age, weight, or body surface area
    DUNGER DB et al. ESPE/LWPES Consensus statement on diabetic ketoacidosis in children and adolescents. Arch Dis Child 2004 Feb
  • 17. Monitoring
    • Blood glucose estimation every hourly
    • Check sr.electrolytes 2 hours after resuscitation is begun and then at least 4 hourly
    • Arterial Blood Gas every 4 to 6 hourly
    British Society of Pediatric and Endocrinology Recommended DKA Guidelines 2009
  • 18. Type of Fluid
    • Initially use 0.9% saline with 20 mmol KCl in 500 ml, and continue this sodium concentration for at least 12 hours.
    • Use crystalloid not colloid
    DUNGER DB et al. ESPE/LWPES Consensus statement on diabetic ketoacidosis in children and adolescents. Arch Dis Child 2004 Feb.
  • 19. Change of fluid
    • Based on..
      • Sodium
      • Blood glucose
      • Potassium
    • After 12 hours,
      • if the plasma sodium level is stable or increasing, change to 500ml bags of 0.45% saline/5% glucose/20 mmol KCl.
      • This will prevent development of hyperchloremic metabolic acidosis
    HARRIS GD et al Minimizing the risk of brain herniation during treatment of diabetic ketoacidemia: a retrospective and prospective study. J Pediatr 1990
  • 20. Sodium
      • if plasma sodium is falling, continue with Normal saline (with or without glucose depending on blood glucose levels).
    HARRIS GD et al Minimizing the risk of brain herniation during treatment of diabetic ketoacidemia: a retrospective and prospective study. J Pediatr 1990
  • 21. Concept of “Corrected Sodium”
    • Sr Osmolality = 2 x (Na+ K) + Bld glucose + BUN
    • True Sodium : For every 100mg% of blood glucose above 100 add 1.6 to the measured Sodium
    • With fluid therapy, the “corrected sodium” should start rising and this should not mean evidence of dehydration. A fall in corrected sodium during therapy is ominous of impending cerebral edema.
    18 1.6 MEL JM et al Incidence and outcome of diabetic cerebral oedema in childhood: are there predictors? J Paediatric Child Health 1995
  • 22. Change of Fluids
    • Glucose
    • During initial volume expansion the plasma glucose concentration falls steeply
    • Thereafter, and after commencing insulin therapy, the plasma glucose concentration should decrease at a rate of 50-100mg/dl/hour
    • Once the blood glucose has fallen to 250mg/dl add glucose to the fluid.
    International Society For Pediatric and Adolescent Diabetes Clinical Practice Consensus Guidelines 2009 Compendium.
  • 23. Solutions
    • The following solutions should be available
    • 500ml bag of 0.45% saline / 5% Dextrose containing 20 mmol KCl
    • 500ml bag of 0.9% saline / 5% Dextrose containing 20 mmol KCl
    • 500ml with 10% dextrose 0.45% saline
  • 24. Oral Fluids
    • In severe dehydration, impaired consciousness & acidosis do not allow fluids by mouth.
    • N/G tube may be necessary in the case of gastric paresis.
    • Oral fluids (e.g fruit juice/oral rehydration solution) should only be offered after substantial clinical improvement and no vomiting
  • 25. Insulin
    • Although rehydration alone causes some decrease in blood glucose concentration (improved renal perfusion will remove sugar osmotically through urine)
    • Insulin therapy is essential to normalize blood glucose and suppress lipolysis and ketogenesis
    LUZI L et al. Metabolic effects of low-dose insulintherapy on glucose metabolism in diabetic ketoacidosis. Diabetes 1988 Nov. KITABCHI AE. Low-dose insulin therapy in diabetic ketoacidosis: fact or fiction? Diabetes Metab Rev 1989 Jun
  • 26. Insulin Therapy
    • Start insulin infusion 1–2 hours after starting fluid replacement therapy; i.e. after the patient has received initial volume expansion
    • Starting Insulin along with the Fluid therapy can bring down the sugars very rapidly leading to osmotic and electrolytic disturbances and is associated with cerebral edema
    EDGE J et al. The UK case-control study of cerebral oedema complicating diabetic ketoacidosis in children. Diabetologia 2006 .
  • 27.
    • Extensive evidence indicates that ‘low dose’ IV insulin administration should be the standard of care
    • An IV bolus is unnecessary may increase the risk of cerebral edema and should not be used at the start of therapy
    EDGE J et al. The UK case-control study of cerebral oedema complicating diabetic ketoacidosis in children. Diabetologia 2006 .
  • 28. Correction of Insulin Deficiency
    • Dose: 0.1 unit/kg/hour (for example, one method is to dilute 50 units regular [soluble] insulin in 50 mL normal saline, 1 unit = 1 mL)
    • Route of administration : IV infusion
    EDGE J et al. The UK case-control study of cerebral oedema complicating diabetic ketoacidosis in children. Diabetologia 2006 .
  • 29. When to Stop Insulin Infusion?
    • DO NOT stop the insulin infusion after blood glucose is being normalised, as insulin is required to switch off ketone production.
    • Once the blood glucose is down to 250mg%, consider reducing the insulin infusion rate, but to no less than 0.05 units/kg/hour.
    • Stop Insulin infusion only after two successive blood gases 4 hours apart show Ph above 7.35 and Bicarbs above 16mEq/L
    British Society of Pediatric and Endocrinology Recommended DKA Guidelines 2009
  • 30. Hypokalemia
  • 31. Intra cellular Hypokalemia
    • Intracellular potassium is depleted because of
      • Increased plasma osmolality causes solvent drag in which water and potassium are drawn out of cells
      • Glycogenolysis and proteolysis secondary to insulin deficiency cause potassium efflux from cells.
    International Society For Pediatric and Adolescent Diabetes Clinical Practice Consensus Guidelines 2009 Compendium.
  • 32. Extra cellular Hypokalemia
    • Due to dehydration there is secondary hyperaldosteronism, which promotes urinary potassium excretion
    • Moreover, administration of insulin and the correction of acidosis will drive potassium back into the cells, decreasing serum levels
    International Society For Pediatric and Adolescent Diabetes Clinical Practice Consensus Guidelines 2009 Compendium.
  • 33. Hyperkalemia
    • In some cases, the Sr. potassium can be elevated if there is associated renal dysfunction, which can reduce potassium excretion
    International Society For Pediatric and Adolescent Diabetes Clinical Practice Consensus Guidelines 2009 Compendium.
  • 34. Potassium Supplementation
    • Replacement therapy is required regardless of the serum potassium concentration
    • If Hypokalemic at admission,
      • Start potassium replacement at the time of initial volume expansion and before starting insulin therapy .
    TATTERSALL RB. A paper which changed clinical practice (slowly). Jacob Holler on potassium deficiency in diabetic acidosis Diabet Med 1999 Dec
  • 35. Potassium supplementation
      • If not very severe hypokalemia, start replacing potassium after initial volume expansion and concurrent with starting insulin therapy.
    • If Hyperkalemic
      • Defer potassium replacement therapy until urine output is documented
  • 36. Phosphate
    • Depletion of phosphate occurs as it is lost in urine due to osmotic diuresis.
    • Hypophosphatemis is further exacerbated by insulin, which promotes entry of phosphate into cells
    International Society of Pediatric and Adolesent Diabetes Clinical Practice Consensus Guidelines 2009 Compendium.
  • 37. Phosphate
    • Prospective studies have not shown clinical benefit from phosphate replacement.
    • As the blood glucose gets corrected and polyuria settles, urinary loss of phosphates stops on its own
    • Only Severe hypophosphatemia in conjunction with unexplained weakness should be treated
    BOHANNON NJ. Large phosphate shifts with treatment for hyperglycemia. Arch Intern Med 1989 Jun: 149(6): 1423–5.
  • 38. Acidosis and Bicarbonate
    • Severe acidosis is reversible by fluid and insulin replacement
    • Insulin stops further ketoacid production and allows ketoacids to be metabolized, which generates bicarbonate
    • Treatment of Hypovolemia improve tissue perfusion and renal function, thereby increasing the excretion of organic acids.
  • 39. Acidosis and Bicarbonate
    • Controlled trials have shown no clinical benefit from bicarbonate administration
    • Bicarbonate therapy may cause
      • paradoxical CNS acidosis (production of H2O and CO2.The CO2 enters the BBB and forms carbonic acid)
      • rapid correction of acidosis with bicarbonate can aggravate hypokalemia
    OKUDA Y et al . Counterproductive effects of sodium bicarbonate in diabetic ketoacidosis. J Clin Endocrinol Metab 1996
  • 40. Acidosis and Bicarbonate
    • Selected patients who may benefit from cautious alkali therapy.
      • Severe acidemia (arterial pH <6.9) in whom decreased cardiac contractility and peripheral vasodilatation can further impair tissue perfusion, and
      • Life-threatening hyperkalemia
    • If bicarbonate is considered necessary, cautiously give 1–2 mEq/kg over 60 minutes
    OKUDA Y et al . Counterproductive effects of sodium bicarbonate in diabetic ketoacidosis. J Clin Endocrinol Metab 1996
  • 41. Deep Vein Thrombosis
    • The Intracranial venous sinuses
    • Femoral vein thrombosis in young and very sick children who have femoral lines inserted.
    • Therefore consideration should be given to anticoagulating these children with 100 units/kg/day as a single daily dose of Fragmin.
    British Society of Pediatric and adolescent Diabetes Recommended DKA Guidelines 2009
  • 42. Infections
    • Systemic Infections – Antibiotics are not given as a routine unless a severe bacterial infection is suspected
    British Society of Pediatric and adolescent Diabetes Recommended DKA Guidelines 2009
  • 43. Changeover to SC Insulin
    • When ketoacidosis has resolved, oral intake is tolerated, and the change to SC insulin is planned
    • To prevent rebound hyperglycemia the first SC injection should be given 15–30 minutes (with rapid- acting insulin) or 1–2 hours (with regular insulin) before stopping the insulin infusion to allow sufficient time for the insulin to be absorbed
    DELLA MANNA T, et al. Subcutaneous Use of a Fast-Acting Insulin Analog: An alternative treatment for pediatric patients with diabetic ketoacidosis. Diabetes Care 2005 Aug
  • 44. Hypoglycemia
    • One of the most Common acute complications of the treatment of type 1 diabetes
    • 8 to 30 episodes per 100 patients per year
    • Most dangerous acute complication
    ROSILIO M, et al. Factors associated with glycemic control. A cross-sectional nationwide study in 2,579 French children with type 1 diabetesDiabetes Care 1998 .
  • 45. Hypoglycemia Signs and Symptoms
    • Neuroglucopenic cerebral dysfunction
      • Confusion
      • Drowsy
      • Disoriented
      • Coma
      • Agitated
      • Symptomatic usually at 40 to 50 mg/dl
    • Autonomic (Adrenergic)
      • Sweat
      • Tremor
      • Warm sensation, weakness
      • Hunger
      • Palpitations
      • Tachycardia
      • Dizziness
      • Pale cool skin
    HELLER SR. Abnormalities of the electrocardiogram during hypoglycaemia: the cause of the dead in bed syndrome? Int J Clin Pract Suppl 2002
  • 46. Mild Hypoglycemia
    • Treatment should be provided
      • Promptly
      • immediate oral,
      • rapidly absorbed
    • Give glucose tablets/sugar lumps or a sweet drink (glucose/sucrose drinks, cola etc.)
    International Society of Pediatric and Adolesent Diabetes Clinical Practice Consensus Guidelines 2009 Compendium.
  • 47. Severe
    • Urgent treatment is required.
    • Severe hypoglycemia with loss of conscious-ness ± convulsions (particularly if there is vomiting)
    • Most safely and rapidly reversed by
      • Inj Glucagon
        • 0.5 mg for age <12 yr,
        • 1.0 mg for ages > 12 yr, or
        • 10 – 30 mcg/kg body weight
    International Society of Pediatric and Adolesent Diabetes Clinical Practice Consensus Guidelines 2009 Compendium.
  • 48. Severe
    • If glucagon is unavailable or recovery is inadequate.
    • Intravenous dextrose should be administered by trained personnel over several minutes
      • Dextrose 10 – 25% at a dose of 2 – 5ml/kg
    • Rapid administration, or excessive concentration, i.e., dextrose 50%, may result in an excessive rate of osmotic change
    International Society of Pediatric and Adolesent Diabetes Clinical Practice Consensus Guidelines 2009 Compendium.
  • 49. Assesment
    • Every hypoglycemic episode should be assessed carefully to determine its cause
      • evaluating the insulin action profile (time of insulin adminis-tration, peak insulin action, and intensity of insulin action)
      • recent food intake (timing and amount of carbohy-drates eaten and peak BG effect of recent food);
      • recent physical activity (timing, duration, and intensity).
    International Society of Pediatric and Adolesent Diabetes Clinical Practice Consensus Guidelines 2009 Compendium.
  • 50. Summarise
    • Know the importance of early detection of DKA
    • Slow correction of dehydration
    • Not taking 10% dehydration for calculations and not using Holiday Segar formula for maintenance fluid calculations
    • Watching “corrected Sodium” trends
  • 51.
    • Avoid Insulin Bolus and Bicarbonate therapy
    • Avoiding to start Insulin along with the initial fluid resuscitation
    • Anticoagulant prophylaxis
    • Administration of Potassium in IV fluids even in the initial bolus therapy if required
  • 52. THANK YOU

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