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diabetic ketoacidosis DKA

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this power point descripe diabetic ketoacidosis in pediatric age group .. we talk about the risk of it .. management specially (fluid management) as case study .. complications and the treatment of brain oedema .. i hope to be auseful one .. enjoy

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diabetic ketoacidosis DKA

  1. 1. Diabetic ketoacidosis Presented by : Yusor jaafar Supervised by : Dr.Haider
  2. 2. Difinition • Hyperglycemia (blood glucose >11 mmol/L [200 mg/dL]) • Venous pH <7.3 and/or bicarbonate <15 mmol/L • Ketonemia and ketonuria http://cdn.intechopen.com/pdfs-wm/42614.pdf
  3. 3. Epidemiology • Type I D.M. Increase to 5.4% annually according to jouvenile diabetes research foundation .. Third of them complain from DKA . • The incidence of DKA is 4.6-8.0 per 1000 person-years • the mortality rate is 1-2%. • The risk of DKA in established T1DM is 1–10% per patient per year • http://cdn.intechopen.com/pdfs-wm/42614.pdf
  4. 4. Essential Pathophysiology of DKA: 1. Absolute or relative deficiency of insulin 2. Resultant excess of counter-regulatory hormones 3. Increased hepatic glucose production and diminished glucose uptake by peripheral tissues cause the hyperglycemia in DKA leading to glycosuria, osmotic diuresis and dehydration
  5. 5. Insulin
  6. 6. Keton body
  7. 7. Hyperglycemia Blood glucose concentrations >~500 mg/dL generally indicate sever dehydration~5-9% Glucose ~600 mg/dL: ~25% reduction in GFR Glucose ~800 mg/dL: ~50% reduction in GFR http://imgpublic.mci-group.com/ie/ICEM2012/Friday/track5/Nathan_Kuppermann.pdf
  8. 8. Acidosis • Anion gap = [Na+ – (Cl- + HCO3-); • normal anion gap = 12. • Acetoacetate is converted to acetone by a spontaneous nonenzymatic process. • Ketone body(ketoacid ,acetoacetate ,betahydroxybutyrate)
  9. 9. Fluid-electrolyte imbalance • Hyperglycemia induces osmotic diuresis leading to total body water deficit often to 10-15% of body weight. • Deficits of electrolytes: • Na+: 5-13 mmol/kg • Cl-: 3-7 mmol/kg • K+: 3-15 mmol/kg • PO4/Mg/Ca++: 1-2mmol/kg • http://peds.stanford.edu/Rotations/picu/pdfs/25_DKA.pdf
  10. 10. K+ • There is profound total body [K+] depletion in DKA. • At the time of presentation, however, plasma [K+] is normal or elevated because of the shift that occurs from intracellular to extracellular space. • http://peds.stanford.edu/Rotations/picu/pdfs/25_DKA.pdf
  11. 11. K+ decrease becauseK+ increase because Inadequate oral intakeAcidosis EmesisHyper glycemia Osmotic diuresisProteolysis
  12. 12. PO4/Mg/Ca++ • Profound hypophosphatemia often occurs in DKA resulting in depressed levels of erythrocyte 2,3-DPG which decreases the P50 of oxyhemoglobin (shifts the oxyHb curve leftward increasing O2 affinity). • PO4++ replacement can result in decreased levels of Mg/Ca++. • http://peds.stanford.edu/Rotations/picu/pdfs/25_DKA.pdf
  13. 13. Case management • 12 year old male,presented to ED with fatigue ,lethargy,confusion with S.O.B,with no medication or chronic medication history and no allergic history
  14. 14. Clinically • Emaciated, weight =25kg • P 140 BP 70/40 RR 45 Temp 37.6°C • Glucose: 36 mmol/l • Acidotic breathing, shocked • CNS – drowsy, but rousable, orientated to person, not place or time
  15. 15. Lab assessment •Urine Ketones + BUN =40 Na=127mmol/l –pH 7.05 –pCO2 1.8 –pO2 18 –Bicarb 5.2
  16. 16. Lab results
  17. 17. Diagnosis
  18. 18. ABC Secure the airway and empty the stomach by continuous nasogastric suction to prevent pulmonary aspiration, in case there is deterioration in conscious level.
  19. 19. A peripheral intravenous (IV) catheter should be placed for convenient and painless repetitive blood sampling. An arterial catheter may be necessary in some critically ill pa‐ tients managed in an intensive care unit.
  20. 20. • Perform continuous electrocardiographic monitoring to assess T-waves for evidence of hyper- or hypokalemia • Give oxygen to patients with severe circulatory impairment or shock
  21. 21. • Give antibiotics to febrile patients after obtaining appropriate cultures of body fluids • Catheterize the bladder if the child is unconscious or unable to void on demand (e.g., in‐ fants and very ill young children)
  22. 22. Fluid &electrolytes • Restoration of circulating volume • Replacement of sodium and the ECF and intracellular fluid deficit of water • Improved glomerular filtration with enhanced clearance of glucose and ketones from the blood • Reduction of risk of cerebral edema
  23. 23. Rehydration•for this patient Normal (0.9%) Saline Weight =25kg Maintenance =1600ml Deficit =25*100=2500ml (sever dehydration 10%) Requirement = 4100 ml
  24. 24. Type of fluid • Normal (0.9%) Saline •Generally recommended fluid •Concerns about hyperchloraemic acidosis • Consider 0.45% saline for rehydration if hypernatraemic • http://academic.sun.ac.za/emergencymedicine/powerpoint/15%20281009/DKA%20Case.pptx
  25. 25. • To prevent an unduly rapid decrease in plasma glucose concentration and hypoglycemia, 5% glucose should be added to the IV fluid (e.g., 5% glucose in 0.45% saline) when the plasma glucose falls to approximately 250–300 mg/dL, or sooner if the rate of fall is pre‐ cipitous.
  26. 26. Ringers Lactate
  27. 27. Because • 1)hypotonic saline = increase risk of cerebral oedema • 2)cintain k+ • 3)lactate converted to glucose
  28. 28. Fluid volume •≤ 10ml/kg boluses repeat to max 3 doses (30ml/kg) •Fluid bolus not required if not shocked •Fluid deficit replacement over 24-48 hrs •Lower fluid boluses associated with lower incidence of brain herniation http://academic.sun.ac.za/emergencymedicine/powerpoint/15%20281009/DKA%20Case.pptx
  29. 29. Insulin • Insulin is essential in switching off lipolysis and ketogenesis. In dose of (0.1 unit /kg/h) • I.V. bolus doses of insulin at the start of therapy are unnecessary and may increase the risk of developing cerebral oedema.
  30. 30. For this patient • I.v. Insuline =0.1*25=2.5 unit/kg/hr • Repeated blood glucose every one hour. • The fall of blood glucose should not exceed 100 mg per hour. If blood glucose drops more than 100 mg/hr, re‐ duce insulin infusion to 0.05 U/kg/hr. Aim to keep blood glucose at about 11 mmol/L (200 mg/dL) until resolution of DKA
  31. 31. Electrolytes
  32. 32. K+ • Potassium replacement is required in all patients; however, if the serum potassium is .5.5 mmol/ litre, defer giving potassium until it begins to decrease or you have a documented urine output. • Dose =40 mmol/L or 20 mmol potassium/L in the patient receiving fluid at a rate >10 mL/kg/h,at rate of 0.5 mmol/kg/hr.
  33. 33. Bicarbonate
  34. 34. Because • 1)cause intracelluler acidosis • 2)increase risk of cerebral oedema because increase sodium leve in plasma (hypernatremia) • 3)cause cellular hypoxia and hypokalemia
  35. 35. Bicarbonate administration in : • 1)patients with severe acidemia (arterial pH <6.9) • 2)patients with life-threatening hyperkalemia • 1–2 mmol/kg over 60 minutes
  36. 36. Monitoring chart
  37. 37. Switch to oral feeding and S.C. Insuline • Maintanance =0.5 unit/kg/24hr • =12.5 unit / kg/24hr • Morning =8.3 (5.5 lenty+2.7 soluble) • Evening =4.1 (2.7 lenty +1.3 soluble)
  38. 38. Complication 1)Cerebra oedema 2)CNS infarction , venous sinus thrombosis 3)Arrythmia / cardiac arrest/electrolyte abnormality 4)Venous thrombosis ( hypercoagulable state), 50%risk of DVT
  39. 39. • 5)polmunary oedema / ARDS • 6)acute renal failure • 7)bowel ischemia / necrosis / fistula formation
  40. 40. Cerebral edema • Cerebral oedema occurs in up to 1% of all paediatric DKA episodes. • 21-24%of all Pediatric DKA death. • Permanent neurological morbidity: 21-26%
  41. 41. Pathophysiology • Osmotic change
  42. 42. • CNS hypoperfusion / ischemia • Po2 • BUN
  43. 43. Risk factors • Epidemiological factors • Newly diagnosed cases • Young age: < 5 years old • Longer duration of symptoms • Prolonged illness • Extended history of poor metabolic control
  44. 44. • Therapeutic interventions • Rapid rehydration (> 50cc/ kg in first 4 hrs) • Bicarbonate therapy for correction of acidosis • Insulin administration in the first hour of therapy
  45. 45. • Changes in biochemical values during treatment • Severe Hypernatremia • Persistent hyponatremia • An attenuated rise in measured serum sodium concentrations during therapy • Non closure of the anion gap
  46. 46. Diagnostic criteria • Abnormal motor or verbal response to pain • Decorticate or decerebrate posture • Cranial nerve palsy (especially III, IV, and VI) • Abnormal neurogenic respiratory pattern (e.g., grunting, tachypnea, Cheyne-Stokes respiration, apneusis )
  47. 47. Major criteria • Altered mentation/fluctuating level of consciousness • Sustained heart rate deceleration (decrease more than 20 beats per minute) not attributable to improved intravascular volume or sleep state • Age-inappropriate incontinence
  48. 48. Minor criteria • Headache • Vomiting • Diastolic blood pressure >90mmhg • Lethargy • Age <5years
  49. 49. Features at presentation • Severe acidosis (initial pH < 7.1) • Greater hypocapnia after adjusting for degree of acidosis • High Blood urea nitrogen • Severe dehydration • Abnormal mental status
  50. 50. Treatment • Give mannitol 0.5-1 g/kg IV (2.5 ml/kg of 20% solution) over 20 minutes and repeat after 6 hours. • Hypertonic saline (3%), 5-10 mL/kg over 30 minutes.
  51. 51. • Intubation may be necessary for the patient with impending respiratory failure • Elevate the head of the bed. • cranial CT scan should be obtained to rule out other possible intracerebral causes of neurologic deterioration (10% of cases).

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