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Diabetic ketoacidosis/DKA

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Diabetic ketoacidosis/DKA

  1. 1. Dr Amit Shekharay
  2. 2.  Diabetic ketoacidosis (DKA) is the end result of the metabolic abnormalities resulting from a severe insulin deficiency or ineffectiveness.  DKA at diagnosis is more common in young children near the age of five years.
  3. 3. The risk increases gradually in children with  Poor metabolic control  Previous episodes of DKA  Young age  Children with psychiatric and eating disorders  Low socioeconomic status  Low parental education and  Stressful lifestyles.
  4. 4.  Infection (viral fever, pneumonia, UTI etc.), Insulin omission either inadvertently or deliberately, is the cause in most cases.
  6. 6. CLINICAL FEATURES  Children and young people without known diabetes who have increased thirst, polyuria, recent unexplained weight loss or excessive tiredness and any of the following: Nausea or vomiting Abdominal pain Hyperventilation Dehydration Reduced level of consciousness.
  7. 7.  Suspect DKA even if the blood glucose is normal in a child with known diabetes and having above mentioned complains.
  8. 8. DIAGNOSIS 1. Acidosis (indicated by blood pH below 7.3 or plasma bicarbonate below 18 mmol/litre), and 2. Ketonaemia (indicated by blood beta-hydroxybutyrate above 3 mmol/litre) or ketonuria (++ and above on the standard strip marking scale).
  9. 9.  Blood glucose levels are generally high (above 11 mmol/l or 198 mg/dl) but DKA may develop with normal blood glucose.  Urine ketones may be positive long after ketoacidosis has resolved because the nitroprusside reaction routinely used to measure urine ketones by dipstick measures only acetoacetate.
  10. 10.  During DKA, most excess ketones are β- hydroxybutyrate, which increases the normal ratio to acetoacetate from 3 : 1 to as high as 8 : 1.  With resolution of the acidosis, β- hydroxybutyrate converts to acetoacetate,which is excreted into the urine and detected by the dipstick test.
  11. 11.  Therefore, persistent ketonuria may not accurately reflect the degree of clinical improvement and should not be relied on as an indicator of therapeutic failure.
  13. 13. MANAGEMENT FULL CLINICAL ASSESSMENT 1. Consciousness Level-Directly related to degree of acidosis. Hourly GCS monitoring. 2. Full Examination- Look for signs of  cerebral oedema (headache, irritability, bradycardia, rising blood pressure, reducing conscious level, N.B. papilloedema is a late sign.  infection  Ileus 3. Weigh the child-If this is not possible then use the most recent clinic weight as a guideline, or an estimated weight from centile charts.
  14. 14. INITIAL INVESTIGATIONS  Blood glucose  Urea  Electrolytes  Blood gases (venous or capillary)  Near patient blood ketones (beta-hydroxybutyrate) if available (superior to urine ketones).  + /- other investigations only if indicated e.g. PCV and full blood count (leucocytosis is common in DKA and does not necessarily indicate sepsis), CXR, CSF, throat swab, blood culture, urinalysis, culture and sensitivity etc.
  15. 15.  Sepsis should be suspected, if there is  Fever or hypothermia  Hypotension  Refractory acidosis  Lactic acidosis.
  16. 16. GENERAL CARE Secure airway, Give 100% oxygen by face-mask Insert IV cannula and take blood samples Cardiac monitor for T wave Measure blood pressure and heart rate.
  17. 17.  If Reduced level of consciousness and vomiting present think about inserting a NG tube to reduce the risk of aspiration.
  18. 18. Fluid management  Indications for starting fluid  Fluid bolus  Fluid calculations  Type of fluid  insulin
  19. 19. FLUIDS: Children who are alert, not clinically dehydrated, not nauseated or vomiting, do not always require IV fluids, even if their ketone levels are high.
  20. 20.  INITIAL FLUID BOLUS: If child is in shock give 10 ml/kg 0.9% sodium chloride as a bolus.  Do not give further boluses to a child with severe DKA without discussion with the responsible senior paediatrician.
  21. 21. Volume of fluid  Once circulating blood volume has been restored (child is no more in shock), calculate fluid requirements as follows: Requirement = Deficit + Maintenance
  22. 22. Volume of fluid Assume a 5% fluid deficit in mild or moderate DKA (pH>7.1). Deficit – Assume a 10% fluid deficit in severe DKA (pH<7.1). Weight (kg) Maintenance fluid <10 2 ml/kg/hour 10-40 1 ml/kg/hour >40 40 ml/hour Maintenance – Calculate by using the following 'reduced volume' rules
  23. 23. If more than 20 ml/kg NS bolus has been given Subtract any additional bolus volumes from the total fluid calculation for the 48-hour period ie, if 30 ml/kg bolus has been given then subtract 10 ml/kg from the calculations.
  24. 24. Fluid Calculation  Hourly rate = (deficit / 48hr) + maintenance per hour Weight Hourly rate 20 kg, with pH 7.18 without any fluid bolus Deficit= 5% x 20 kg = 1000 mls Rate = 1000÷48= 21ml/hr Maintenance 1ml/kg/hr = 20 ml/hr Total rate= 41ml/hr 50 kg, with pH of 6.8 and required 30 ml/kg 0.9% sodium chloride bolus for circulatory collapse Deficit= 10% x 50 kg= 5000 mls 10 ml/kg bolus fluid = -500mls=4500 mls rate=4500÷48= 93.7 ml/hr Maintenance= 40ml/hr Total rate=133.7 ml/hr
  25. 25. Type of fluid  0.9% sodium chloride with 20 mmol potassium chloride in 500 ml (40 mmol per litre) till blood glucose ˃14 mmol/l (252 mg/dl).  Do not give oral fluids to a child who is receiving intravenous fluids for DKA until ketosis is resolving and there is no nausea or vomiting.  .
  26. 26.  If oral fluids are given before the 48hr rehydration period is completed, the IV infusion needs to be reduced to take account of the oral intake.
  27. 27. INSULIN  0.05 to 0.1 units/kg/hour, 1-2 hours after beginning intravenous fluid therapy (cerebral oedema is more likely if insulin is started early).  Once the blood glucose has fallen to 14 mmol/l (252mg/dl), add glucose to the fluid and think about the insulin infusion rate, as follows –
  28. 28.  If ketone levels are < 3 mmol/l  change the fluid to contain 5% glucose  Reduce to or maintain at an insulin infusion rate of 0.05 units/kg/hr  If ketone levels are > 3 mmol/l  Maintain the insulin infusion rate at 0.05 to 0.1 units/kg/hour to switch off ketogenesis  Change the fluid to contain 10% glucose
  29. 29.  Blood glucose ˂ 6 mmol/l (108mg/dl)- increase the glucose concentration of ivf, and if there is persisting ketosis, continue insulin with at least 0.05 units/kg/hour.  Blood glucose ˂ 4 mmol/l (72 mg/dl), give a bolus of 2 ml/kg of 10% glucose and increase the glucose concentration of the infusion. Insulin can temporarily be reduced for 1 hour.
  30. 30.  If the blood beta-hydroxybutyrate level is not falling within 6–8 hours in a child with DKA, think about increasing the insulin dosage to 0.1 units/kg/hour or greater.
  31. 31.  Once the pH is > 7.3, ketones are <3, the blood glucose is down to 14 mmol/l (252 mg/dl), and a glucose-containing fluid has been started, reduce the insulin infusion rate, to 0.05 units/kg/hour.
  32. 32.  If acidosis is not correcting, consider the following  Insufficient insulin to switch off ketones  Inadequate resuscitation  Sepsis  Hyperchloraemic acidosis  Salicylate or other prescription or recreational drugs
  33. 33.  Think about stopping intravenous fluid therapy when ketosis is resolving and oral fluids are tolerated without nausea or vomiting.  Start subcutaneous insulin at least 30 minutes before stopping intravenous insulin.  If the child was using insulin pump therapy, restart the pump at least 60 minutes before stopping intravenous insulin.
  34. 34. POTASSIUM  All fluids (except any initial bolus) contain 40 mmol/l potassium chloride, unless there is evidence of renal failure.  Hypokalaemia (potassium below 3 mmol/litre): think about temporarily suspending the insulin infusion
  35. 35. SODIUM “True,” serum sodium= [ Na+] + (1.6 mEq/L Na+ for every 100 mg/dL glucose in excess of 100) Corrected sodium levels should rise as blood glucose levels fall during treatment. If the child is becoming hypernatraemic, this is not generally a problem, and is protective against cerebral oedema.
  36. 36. BICARBONATE  Not required.
  37. 37. MONITORING CONTINUOUS EVERY 30 MINUTES (in children under 2 years with DKA and children with severe DKA) [high risk of cerebral oedema] HOURLY 2 HRS AFTER STARTING AND THEN 4 HOURLY ECG (to detect signs of hypokalaemia) Level of consciousness (using the modified Glasgow coma scale) Capillary blood glucose Glucose (laboratory measurement) Heart rate (to detect bradycardia) Vital signs (heart rate, blood pressure, temperature, respiratory rate [look for Kussmaul breathing]) Blood pH and pCO2 Fluid balance, with input and output charts Plasma sodium, potassium and urea Level of consciousness Beta- hydroxybutyrate.
  38. 38. COMPLICATIONS  Headache,  Agitation or irritability  Unexpected fall in heart rate  Increased blood pressure and  Signs such as deterioration in level of consciousness  Abnormalities of breathing pattern, for example respiratory pauses  Oculomotor palsies  Abnormal posturing  Pupillary inequality or dilatation  CEREBRAL OEDEMA
  39. 39. COMPLICATIONS  Treat immediately with the most readily available  Mannitol (20% 0.5-1 g/kg over 10-15 minutes), or  Hypertonic saline (2.7% or 3% 2.5-5 ml/kg over 10-15 minutes).  A repeated dose of Mannitol may be required after 2 hours if there is no response, In addition fluids should be restricted to ½ maintenance rates and inform senior staff immediately.
  40. 40. COMPLICATIONS  Hypoglycaemia and hypokalaemia  Systemic Infections: Antibiotics are not given as a routine unless a severe bacterial infection is suspected.  Aspiration pneumonia- Insert NG tube in vomiting child with impaired consciousness
  41. 41. AVOIDING FUTURE EPISODES OF DIABETIC KETOACIDOSIS  Discuss with family members or carers (if appropriate) the factors that may have led to the episode.  Think about the possibility of non-adherence to therapy in children and young people with established type 1 diabetes who present with DKA, especially if the DKA is recurrent.
  42. 42.  Advise how to reduce the risk of future episodes. In particular, advise them of the importance of managing intercurrent illnesses.  Provide appropriate diabetes education and practical information  Emotional and psychological well-being assessment who present with frequent episodes of diabetic ketoacidosis over a relatively short time (previously known as 'brittle diabetes').