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Diabetes Ketoacidosis

Diabetes Ketoacidosis. Dr Hessa Al Kandari Pediatric Endocrinologist Farwania Hospital. Pathophysiology. Absolute /relative Insulin . Counterregulatory hormones ( glucagon, GH, cortisol , epinephren ) . catabolic state. glycogenolysis Gluconeogeneis Lipolysis ketogenesis.

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Diabetes Ketoacidosis

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  1. Diabetes Ketoacidosis Dr Hessa Al Kandari Pediatric Endocrinologist Farwania Hospital

  2. Pathophysiology Absolute /relative Insulin Counterregulatory hormones ( glucagon, GH, cortisol, epinephren) catabolic state glycogenolysis Gluconeogeneis Lipolysis ketogenesis Hyperglycemia Ketonemia Metabolic acidosis

  3. Pathophysiology • severe depletion of water and electrolytes from intra- and extracellular fluid compartments • At presentation, magnitude of specific deficits depending • duration and severity of illness • the extent to which patient able to maintain intake of fluid and electrolytes • content of food and fluids consumed . • Consumption of fluids with a high-carbohydrate content (juices or sugar containing soft drinks) exacerbate the hyperglycemia .

  4. Biochemical criteria Hyperglycemia (BG>11 mmol/L) VenouspH <7.3 or HCO3<15 mmol/L Ketonemiaand ketonuria.

  5. Severity categorization • Mild: venous pH <7.3 or HCO3<15 mmol/L • Moderate: pH <7.2, HCO3<10 mmol/L • Severe: pH <7.1, HCO3<5 mmol/L

  6. Clinical manifestations Dehydration Rapid, deep, sighing (Kussmaul respiration) Nausea, vomiting, abdominal pain Progressive obtundation and loss of consciousness

  7. Epidemiology 677 diabetic children 12 yr , diagnosed during the period of 2000 -2006 37.7% DKA at presentation. 74.1% mild / moderate DKA. 83% of children with severe DKA were in the 0-4 yr age . 4% needed ICU care. One child (0.15%) died cerebral edema. Abdul Rasoul et al 2010 , Pediatric Diabetes,2010 Aug;11(5):351-6

  8. Epidemiology DKA at diagnosis common • <5 years of age • families do not have ready access to medical care. DKA in established T1DM • poor metabolic control / previous episodes of DKA • peri-pubertal / adolescent girls • psychiatric disorders/ unstable family circumstance • insulin omission or failure to follow sick day or pump failure management guidelines accounts for almost all episodes.

  9. Case 1 10 y/o girl, diagnosed DM1 since age of 8 yrs on insulin glargine 10 IU and premealactrapid 4 IU . Had regular follow up; last HbA1C was 9%. Presented to the ER with H/O fever and runny nose for 2 days and abdominal pain and vomiting for 1 day. Mom admitted omitting one dose of insulin (glargine) child has poor appetite. Examination : conscious with acetone smell breath, congested throat and dry mucous membranes.

  10. Management plan • clinical evaluation to confirm diagnosis and determine its cause • look for evidence of infection. • Weigh the patient. This weight used for calculations and not the weight from a previous office visit or hospital record. • Assess clinical severity of dehydration. ( Clinical assessment of dehydration is imprecise, inaccurate and generally shows only fair to moderate agreement among examiners). • Assess level of consciousness (Glasgow coma scale)

  11. Management plan • urinalysis for ketones. • Measurement of ß-hydroxybutyrate (if available) confirm ketoacidosis & to monitor response • specimens for culture (blood, urine, throat). • If lab K measurement delayed,doECG (evaluation of K status)

  12. Management plan blood sample for laboratory measurement • serum or plasma glucose • Electrolytes, BUN creatinine, osmolality • venous (arterial in critically ill patient) pH, pCO2 • Ca, Pho, mg(if possible) • HbA1c, • CBC

  13. Case 1 HR110/min, RR 35/min, BP 100/60 Temp 38.5 C. Her current wt 30 KG. • Bedside Urine dipstick: glucose +4, ketones +3. • Capillary Blood gas: PH 7.19, HCO3: 9, PO2: 10 kpa, PCO2: 3 Kpa. • RBG 24 mmol/l. • Na 130 mmol/L, K 4.5 mmol/L, urea 7 mmol/L, creatinin 70 mmol/L.

  14. Case 1 • moderate DKA. • Omitting insulin dose • Upper respiratory tract infection. • failure to adherence to sick days management guidelines • What is the diagnosis? • What precipitated the acute condition?

  15. Goals of therapy • Correct dehydration • Correct acidosis and reverse ketosis • Restore blood glucose to near normal • Avoid complications of therapy • Identify and treat any precipitating event

  16. Case 1 What is your further management plan?

  17. Further clinical and biochemical monitoring • Successful management of DKA requires meticulous monitoring of the patient’s clinical and biochemical response to treatment so that timely adjustments in treatment can be made when indicated by the patient’s clinical or laboratory data . • There should be documentation on a flow chart of hour-by-hour clinical observations, IV and oral medications, fluids, and laboratory results.

  18. Where should the child be managed? The child should receive care in a unit that has: • Experienced nursing staff • Written guidelines for DKA management in children • Access to laboratories that can provide frequent and timely measurements of biochemical variables • A specialist /consultant pediatrician with training and expertise in the management of DKA should direct inpatient management.

  19. Monitoring • Hourly vital signs • Hourlyneurological observations (GSC) • Hourly fluid input (including all oral fluid) and output. • Hourly Capillary blood glucose( cross-checked against lab). • Laboratory tests 2-hourly for the first 12 hours : serum electrolytes, glucose, BUN, Ca, Pho,mg,Hct and blood gases repeated, more frequently, as indicated. • every2 hours Urine ketones until cleared or blood(BOHB) if available.

  20. Supportive measures Secure the airway deterioration in conscious level: NGT suction. peripheral (IV) catheter : convenient . oxygen :circulatory impairment or shock. Antibiotics: febrile patients after cultures . Bladder catheterization not necessary ( unconscious or unable to void on demand )

  21. Type fluid? • Calculate Rate? • Insulin rate?

  22. Principles of Water and Salt Replacement The principles were developed after a comprehensive review of the literature and were accepted and endorsed by a panel of expert physicians representing the LWPES, ESPE, and ISPAD. Pediatric Diabetes 2009: 10(Suppl. 12): 118–133

  23. Fluids and salt • moderate DKA use 5–7% ; severe DKA7–10% dehydration • IV /oral fluids given in another facility should be factored into calculation of deficit. • severe volume depletion, begin immediately with 0.9% saline,10 mL/kg/h over 1–2 hrs, may be repeated. • In shock, isotonic saline (or Ringer’s lactate) 20 mL/kg boluses infused as quickly as possible.

  24. Fluids and salt • Subsequent fluid management should be with 0.9% saline or Ringer’s acetate for at least 4–6 hours. • Thereafter ,with solution that has a tonicity ≥ 0.45% saline with added potassium chloride, potassium phosphate or potassium acetate • Urinary losses not routinely be added. • rehydrate evenly over 48 hours ( a rate rarely of 1.5–2X daily maintenance).

  25. Correction of insulin deficiency • insulin to normalize BG and suppress lipolysis & ketogenesis • ‘low dose’ IV insulin is the standard of care . • insulin infusion 1–2 hours after fluid replacement therapy. • Dose: 0.1 unit/kg/hour • IV bolus may increase risk of cerebral edema • insulin remain at 0.1 unit/kg/hour at least until resolution of DKA (Ph >7.30, bicarbonate >15 mmol/L and/or closure of the anion gap), which takes longer than normalization of BG.

  26. Correction of insulin deficiency • During initial volume expansion BG falls steeply . • Thereafter, BG decreases at a rate of 2–5 mmol/L/hour. • D5% should be added to IV when the BG falls to 14–17 mmol/L, or sooner if BG falls (>5 mmol/L/h) after initial fluid expansion. • Use D10% or D12.5% to prevent hypoglycemia while continuing insulin to correctacidosis. ( keep BG≈11 mmol/ until resolution of DKA). • In marked insulin sensitivity, dose may be decreased to 0.05 unit/kg/hr, or less, provided acidosis ct resolving.

  27. Acidosis • Severe acidosis is reversible by • fluid (improves renal function, increasing the excretion of organic acids). • insulin (stops ketoacid production and allows ketoacids to be metabolized, which generates bicarbonate) • Controlled trials no benefit from bicarbonate administration (paradoxical CNS acidosis, hypokalemia, increasing osmolality)

  28. Acidosis • Bicarbonate administration is not recommended unless the acidosis is profound and likely to affect adversely the action of adrenaline/epinephrine during resuscitation. • selected patients 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 • patients with life-threatening hyperkalemia • If necessary, cautiously give 1–2 mmol/kg over 60 min .

  29. Case 2 1 yr 10 months old girl previously healthy presented to the emergency room with H/O poly urea, polydypsia of 2 wks duration, and irritability and abdominal pain for 1 day prior to admission. Examination :drowsy (GCS 13), RR 40/mint, pulse rate: 142/mint; BP 80/50 mmHg, capillary refill 3-4 sec. Deep breathing, acetone smell breath, severe dehydration and diaper rash.

  30. Case 2 • Glucocheck : 30 mmol/L • Urine : Glucose ++++, Ketones ++++ • Capillary blood gas analysis: Ph 7; HCO3 3.8mmol/L; Pco2 2.1 Kpa. • Na 142 mmol/L; K 5 mmol/L, urea 8 mmol/L.

  31. Case 2 What is your management plan?

  32. PICU increased risk for cerebral edema <5 years severe acidosis low pCO2 high BUN

  33. Case 2 Patient was started on normal saline bolus repeated and started insulin infusion at a rate of 0.1 unit/kg/hour according to hospital protocol; reassessed after 4 hours : the ph 7 and HCO3 4? What actions will you take? • Check hydration status • Check preparation of IVF, calculation of rate, insulin preparation & rate. • Look for signs of infection

  34. Case 2 After 7 hours the K dropped to 3.4 mmol/l, Phos 0.6 mmol/l while child was on NS with 40meq/l KCL. How will this affect your management plan?

  35. Potassium replacement In DKA total body potassium deficits 3 to 6 mmol/kg, but potassium levels may be normal, increased or decreased . • loss from body (vomiting ,osmotic diuresis, secondary hyperaldosteronism) • Insulin, correction of acidosis will drive potassium into cells. Replacement required regardless of the serum potassium level

  36. Potassium replacement • If hypokalemia, start K replacement at time of initial volume expansion and before insulin therapy. • Otherwise, start K after initial volume expansion • If patient hyperkalemic, defer K replacement therapy until urine output is documented. • The starting K concentration 40 mmol/L. Maximum rate 0.5 mmol/kg/hr. • If hypokalemia persists, then insulin infusion rate can be reduced.

  37. Phosphate Depletion of intracellular phosphate (osmotic diuresis) phosphate falls after treatment and this is exacerbated by insulin. Significant hypophosphatemia may occur if IV therapy without food intake ≥24 hrs . Severe hypophosphatemia with unexplained weakness should be treated. Potassium phosphate salts may be used as an alternative to or combined with potassium chloride or acetate, provided careful monitoring of serum calcium to avoid hypocalcemia

  38. Case 2 After 20 hours from admission clinical condition improved . Last blood gas analysis: Ph 7.29, HCO3 14 mmol/L, PCo2 4. IVF is NSD 7.5 with 60 meq/L KCL/Kphospate. Blood glucose 10 mmol/l. Nurse noticed that the child started to be irritable, screaming. She checked her vitals again BP 110/70, HR 70/min. What is the diagnosis? What is your further management ?

  39. Case 2 What are the risk factors for cerebral edema in the patient? • Young age • High urea nitrogen • Severe DKA • Low PCO2

  40. Case 2 • Cerebral edema • Give manitol ; reduce IVF to 2/3 mainainence, raise the head of the bed. • Call the senior intensivest , consultant endocrinologist • Order CT head

  41. Cerebral edema The pathogenesis of both its initiation and progression is unclear and incompletely understood. usually develops 4–12 hrs after treatment , but can occur before treatment has begun or, rarely as late as 24–48 hrs after treatment Demographic factors associated with increased risk of cerebral edema • Younger age • New onset diabetes • Longer duration of symptoms

  42. Epidemiological potential risk factors at diagnosis or during treatmentof DKA • Greater hypocapnia • Increased BUN • More severe acidosis • Bicarbonate treatment • An attenuated rise in measured serum sodium concentrations during therapy • Greater volumes of fluid given in the first 4 hours • Administration of insulin in the first hour of fluid treatment

  43. Warning signs and symptoms of cerebral edema • Headache & slowing of heart rate • Change in neurological status (restlessness, irritability, increased drowsiness, incontinence) • Specific neurological signs (e.g., cranial nerve palsies) • Rising blood pressure • Decreased O2 saturation

  44. Treatment of cerebral edema • Initiate treatment as soon as suspected. • Reduce rate of fluid by one-third. • Give mannitol 0.5–1 g/kg IV over 20 min, repeat if no initial response in 30 min to 2 hrs • Hypertonic saline (3%), 5–10 mL/kg over 30 min, may be an alternative to mannitol or a second line of therapy if there is no initial respons to mannitol .

  45. Treatment of cerebral edema Elevate the head of the bed Intubation may be necessary for the patient with impending respiratory failure, but aggressive hyperventilation (to a pCO2 <2.9 kPa) not recommended( poor outcome) After treatment started, CT scan to rule out other possible intracerebral causes of neurologic deterioration (thrombosis or hemorrhage, benefit from specific therapy).

  46. Morbidity and mortality • mortality rate 0.15% to 0.30%. • Cerebral edema accounts for 60% to 90% of all deaths • 10% to 25% of survivors of cerebral edemahave residual morbidity. • Electrolyte disturbances and hypoglycemia • CNS complications (DIC, duralsinu thrombosis, basilar artery thrombosis) Peripheral venous thrombosis

  47. Take home messages • DKA is caused by either relative or absolute insulin deficiency. • Children and adolescents with DKA should be managed in centers experienced in its treatment. • Begin with fluid replacement before starting insulin therapy. • Volume expansion (resuscitation) is required only if needed to restore peripheral circulation.

  48. Take home messages • Subsequent fluid administration (including oral fluids) should rehydrate evenly over 48 hours at a rate rarely in excess of 1.5–2 times the usual daily maintenance requirement. • Begin with 0.1 U/kg/h. 1–2 hours AFTER starting fluid replacement therapy. • If BG decreases too quickly or too low before DKA has resolved, increase the amount of glucose administered. Do NOT decrease insulin infusion

  49. Take home messages • Even with normal or high levels of serum potassium at presentation, there is always a total body deficit of potassium. Begin with 40 mmol potassium/L in the infusate. • No evidence that bicarbonate is either necessary or safe in DKA. • Have mannitol or hypertonic saline at the bedsid and the dose to be given calculated beforehand. • In profound CNS symptoms, mannitol should be given immediately.

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