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

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Presentation on theme: "Page 1 Diabetes Ketoacidosis Dr Hessa Al Kandari Pediatric Endocrinologist Farwania Hospital."— Presentation transcript:

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

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

3 Page 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 Page 4 Biochemical criteria Hyperglycemia (BG >11 mmol/L) Venous pH <7.3 or HCO3 <15 mmol/L Ketonemia and ketonuria.

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

7 Page 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 Page 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 Page 9 Case 1 10 y/o girl, diagnosed DM1 since age of 8 yrs on insulin glargine 10 IU and premeal actrapid 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 Page 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 Page 11 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, do ECG (evaluation of K status) Management plan

12 Page 12 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 Management plan

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

15 Page 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 Page 16 What is your further management plan? Case 1

17 Page 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 Page 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 Page 19 Hourly vital signs Hourly neurological 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. Monitoring

20 Page 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 Page 21 –Type fluid? –Calculate Rate? –Insulin rate?

22 Page 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 Page 23 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. Fluids and salt

24 Page 24 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). Fluids and salt

25 Page 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 Page 26 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. Correction of insulin deficiency

27 Page 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 Page 28 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. Acidosis

29 Page 29

30 Page 30 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.

31 Page 31 –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. Case 2

32 Page 32 Case 2 What is your management plan?

33 Page 33 PICU increased risk for cerebral edema <5 years severe acidosis low pCO2 high BUN

34 Page 34 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 Case 2

35 Page 35 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? Case 2

36 Page 36 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

37 Page 37 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. Potassium replacement

38 Page 38 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

39 Page 39 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 ?

40 Page 40 What are the risk factors for cerebral edema in the patient? –Young age –High urea nitrogen –Severe DKA –Low PCO2 40 Case 2

41 Page 41 –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 Case 2

42 Page 42 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

43 Page 43 Epidemiological potential risk factors at diagnosis or during treatment of 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

44 Page 44 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

45 Page 45 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.

46 Page 46 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). Treatment of cerebral edema

47 Page 47 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 edema have residual morbidity. Electrolyte disturbances and hypoglycemia CNS complications (DIC, dural sinu thrombosis, basilar artery thrombosis) Peripheral venous thrombosis

48 Page 48 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.

49 Page 49 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 Take home messages

50 Page 50 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. Take home messages

51 Page 51

52 Page 52 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 (grunting,Cheyne-Stokes respiration)

53 Page 53 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

54 Page 54 Minor criteria Vomiting Headache Lethargy or not easily arousable Diastolic blood pressure >90 mm Hg Age <5 years One diagnostic criterion, two major criteria, or one major and two minor criteria (sensitivity of 92% false positive rate of 4%).

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