1. IN THE NAME OF GOD

2. DKA Management M. Hashemipour بهمن 1395 Pediatric Endocrinologist
Isfahan university of medical sciences
بهمن 1395

3. Case study
کودک 6 ساله ای با وزن 20 کیلو گرم با تنفس تند به اورژانس وارد شده
در بدو ورود
شما چیست؟
PH=6.9 ,CO3H= 5
NA=135
K=5.5
BS=624

4. DKA Defined Plasma glucose >200 mg/dl Arterial pH <7.30
Bicarbonate level <15 mEq/l
ketonemia>3 mmol/L
Moderate ketonuria
Pediatr Clin N Am 2005
Pediatric Diabetes 2014
ISPAD clinical practice consensus guidelines 2014

5. severe moderate mild parameter 10-15 6-10 3-5 <5 <10 <15
Volume deficit(%)
<5
<10
<15
Co3 H
<7.1
<7.2
<7.3 PH
>600
Blood sugar
>30
≥30
≥25
BUN
Pediatric Diabetes 2014
Endocrinology and Metabolism clinics of north America
ISPAD clinical practice consensus guidelines 2014

6. How to Treat DKA

7. How to Assess severity of Dehydration
Prolonged capillary refill time
Abnormal skin turgor
Abnormal respiratory pattern
sunken eyes, absent tears
weak pulses, and cool extremities
level of consciousness
Pediatric Diabetes 2014

8. Lab Measurement Blood gases Blood or urine ketones serum electrolytes
Full blood count
Blood urea nitrogen, creatinine
Serum osmolality
ECG for baseline evaluation of potassium
Pediatric Diabetes 2014

9. The goals of therapy
improvement of circulatory volume and tissue perfusion
Correct acidosis and reverse ketosis
slowly Reduction of serum glucose and plasma osmolarity

10. The goals of therapy
identification and prompt treatment of comorbid precipitating causes.
correction of electrolyte imbalance
Improved glomerular filtration
increase clearance of glucose and ketones from the blood

11. کودک 6 ساله ای با وزن 20 کیلو گرم با تنفس تند به اورژانس وارد شده
در بدو ورود
PH=6.9 ,CO3H= 5
NA=135
K=5.5
BS=624

12. چه درجه ای از DKA مطرح است
درمان را چگونه آغاز می کنید؟
کنترل قند خون با انسولین چگونه است؟
قند خون در چه سطحی باید حفظ شود؟
میزان ونوع مایع دریافتی به بیمار چگونه خواهد بود؟

13. Severe DKA

14. Step1
Fluid Therapy

15. Step2
Evaluation of predisposing factors

16. Step3
Adding K to IV fluid after urination

17. Step4
Insulin therapy

18. Step5
Bicarbonate therapy??????

19. Step6
Monitoring
Vital sign
Level of consciousness

20. Volume Expansion Shock? 0.9% NaCl 20 ml/kg bolus. Repeat if necessary
No Shock
0.9 % NaCl 10 ml/kg /h over 1-2 hours

21. Volume Expansion Repeated if Shock Hypotension
Delay capillary refilling
Decrease tissue perfusion
Not exceed 30 ml/kg

22. Fluid therapy
Maintenance
Deficit
Abnormal ongoing loss

23. Fluid deficit Grade of dehydration 5% to 10%
In mild to moderately DKA, fluid deficits 30 to 50 mL/kg.
In moderate to severe DKA, fluid deficits 50 to 100mL/kg.

24. Fluid therapy To replace the estimated fluid deficit evenly
Over h.
ISPAD clinical practice consensus guidelines 2014

25. Milwaukee formula Iv rate= 85cc/kg+maintenance- bolus÷ 23hr
Iv rate= 85* ÷ 23hr
Iv rate= 126 cc /hr
Nelson 2014

26. Second Method First day 1.5-2 times the 24 h maintenance requirements
with isotonic solution 0.9% saline,Ringer’s lactate for at least 4–6 h
Then half salin 0.45% salin
Pediatric Diabetes 2014
ISPAD clinical practice consensus guidelines 2014

27. second Method WT= 20kg Maintenance =1500cc
Fluid requirement for DKA=2*1500
Fluid requirement for DKA=1.5*1500

28. Pediatric Fluid therapy
Usually 1.5 times the 24 h maintenance requirements
Urinary losses should not be added to the calculation of replacement fluids
Pediatrics 2004;113;
Pediatric Diabetes 2014
ISPAD clinical practice consensus guidelines 2014

29. Third method Begin with 0.9% NaCl. Weight (kg) Infusion rate (ml/kg/h)
4 –
10 –
20 –
ISPAD clinical practice consensus guidelines 2014

30. Forth method No transport available ORS 5 ml/kg/h
Give . as fruit juice or coconut water if ORS is not available.
Give SC insulin 0.05 U/kg every 1-2 hours
0.025 U/kg if < 5 years
ISPAD clinical practice consensus guidelines 2014

31. Improved condition?
Decreasing blood glucose AND decreasing ketones in urine indicate resolving of acidosis

32. ساعت 6 درمان قند خون بیمار 250 است نوع و میزان مایع 6 ساعت بعدی را بنویسید

33. Second Method Iv rate= 85cc/kg+maintenance- bolus÷ 23hr
Iv rate= 85* ÷ 23hr
Iv rate= 126 cc /hr

34. مایع 6 ساعت بعدی
126*6 = 756 cc
دکستروز5% همراه با 75 میلی اکی والان سدیم درلیتر
در واقع در مایع فوق 56 میلی اکی والان سدیم باید باشد
بنابر این در مایع فوق 81 سی سی سدیم کلراید 20% می ریزیم
هر 1 سی سی سدیم کلراید 20% حاوی 3.2 میلی اکی والان سدیم است

35. Fluid therapy
Dextrose 5% was added in 0.45% NS to the rehydrating solution once the blood glucose fell to mg/dL
Pediatr Crit Care Med 2004
Endocrinol Metab Clin N Am 2006
Pediatric Diabetes 2014
ISPAD clinical practice consensus guidelines 2014

36. Glucose concentration during DKA
plasma glucose typically decreases
At a rate of mg /dl/h
Depending on the timing and amount of glucose administration

37. When we add dextrose?
If blood glucose falls very rapidly >90 mg/dl/h) after initial fluid expansion
Consider adding glucose even before plasma glucose has decreased to 300 mg/dl

38. When we add dextrose? Acidosis with BS 100-200mg/dl
Add%7.5 dextrose to solution
Insulin should be continue

39. When we add dextrose? Acidosis with BS <100mg/dl
Add%10 dextrose to solution
Insulin should be continue

40. When we discontinue intravenous fluids?.
Administration of intravenous fluids should be continued until acidosis is corrected and a patient can tolerate fluids and food.
Pediatr Clin N Am 52 (2005) 1147– 1163

41. Fluid therapy
Maintain the blood glucose
100 and 200 mg/dL.

42. When we added potassium?
At same time as insulin treatment
After urination
Pediatr Crit Care Med 2004 Vol. 5, No. 5

43. Potassium
The plasma potassium concentration should be rechecked every 1 to 2 hours if the plasma concentration is outside the normal range.

44. Potassium potassium 40meq/li
k<3mEq/l insulin should be hold temporary
Give mmol/kg/h iv and oral
Endocrinol Metab Clin N Am 35 (2006) 725–751

45. K>5 meq/l
Don’t give K till reversal of k<5meq/l

46. Indication of Bicarbonate therapy
life-threatening hyperkalemia.
severe acidosis pH<6.9
Hypotension
shock
Arrhythmia

47. Bicarbonate Therapy After 2-3hours of hydration if severe acidaemia
pH <7.0 or bicarbonate <5 mEq
A state of shock
it may be appropriate to use bicarbonate
Give 1meq/kg over 1 hour
ISPAD clinical practice consensus guidelines 2014

48. Biochemical& Clinical monitoring
Critical Observations
Hourly blood glucose
Hourly fluid input & output
Neurological status at least hourly
Electrolytes 2 hourly after start of IV therapy
Monitor ECG for T-wave changes

49. Biochemical& clinical monitoring
Repeated 2–4 h, or more frequently, as clinically indicated

50. insulin therapy Begin with 0.05–0.1 U/kg/h
1–2 h after starting fluid replacement therapy

51. insulin therapy IV dose 0.1 U/kg/h (0.05 U/kg if < 5 years SC or IM
Every 1-2 hours
Dose 0.1 U/kg
(0.05U/kg if < 5 years
ISPAD clinical practice consensus guidelines 2014

52. Insulin therapy
The administration of insulin without fluid replacement in such patients with hypotension may aggrevate
Hypotension
Shock
Hypokalemia
Cerebral oedema

53. درمان وریدی با انسولين روش اول– مداوم
درمان وریدی با انسولين
روش اول– مداوم
ابتدا در cc50 نرمال سالين ، 5واحد انسولين كريستال مي ريزيم و براي بيمارh /0.1iu/kg انسولين شروع مي كنيم تا قند خون به 300 برسد.

54. نرمال سالين را در ميكروست مي ریزیم و هر 60 قطره آن ، cc 1 است .
حال اگر كودكي 20 كيلو باشد و ديابت داشته باشد ، بايد درهر ساعت 20×0/1=2U انسولين بگيرد يعني 20 قطره در دقيقه

55. How long can we continue?
At least until resolution of DKA
pH > 7.30
Bicarbonate > 15 mmol/l
and/or closure of the anion gap
ISPAD clinical practice consensus guidelines 2014

56. When we increase insulin dose?
Not decrease blood ketone
Not decrease anion gap
Not increase PH

57. If the child cannot be transported

58. DKA management with SC &IM insulin
Initial dose SC: 0.3 unit/kg
Followed SC insulin lispro or aspart unit/kg every 2 h.

59. Reduce SC insulin lispro or aspart to 0.05 unit/kg per hour 1-2
if BG falls to <250 mg/dL before DKA has resolved
Reduce SC insulin lispro or aspart to 0.05 unit/kg per hour 1-2
Give glucose-containing fluids orally
To keep BG 200 mg/dL until resolution of DKA
Decreasing urine ketone indicate resolving acidosis

60. انسولين درماني
Mild to moderate DKAدر صورتي که انسولين کريستال یا Novorapid هر 4-2 ساعت زير جلدي تزريق مي کنيم IU/KG

61. Criteria for resolution of DKA includes
Glucose <200 mg/dl
Serum bicarbonate 18 mEq/l
Venous pH of >7.3.

62. Time of feeding If
The patient wishes
Conscious
No vomiting

63. Successful Treatment Assess Reassess Assess again Flow sheets
Consider CVP monitoring

64. پس از خروج از کتواسیدوزیس چه می کنید ؟
بهتر است بر اساس غلظت قند خون تصمیم گیری کنیم
انسولين کريستال یا Novorapid هر 4 ساعت زير جلدي تزريق مي کنيم

65. هر 4 ساعت طبق Scale زيرباید انسولین دريافت كند
180 ≤ BS < kg0/1 واحد S/C
300 ≤ BS < kg/0/15 واحد S/C
BS ≥ kg0/2 واحد S/C

66. To prevent rebound hyperglycemia
The first SC injection should be given
15–30 min with rapid acting insulin
1–2 hr with regular insulin
Before stopping the insulin infusion to allow sufficient time for the insulin to be absorbed

67. WARNING SIGNS BG falls >90 mg/dL/hour Decreased oxygen saturation
Slowing heart rate
Irritability
Decreased conscious level
incontinence
Hypoglycemia

68. Warning signs and symptoms of cerebral edema
Change in neurological status
specific neurological signs (cranial nerve palsies)
Headache
Recurrence of vomiting

69. Warning signs and symptoms of cerebral edema
Decrease more than 20 beats/min) not attributable to improved intravascular volume or sleep state
Rising diastolic blood pressure>90mmHg

70. Risk factors of cerebral edema
A failure of measured serum sodium levels to rise or a further decline in serum sodium levels with therapy is thought to be a potentially ominous sign of impending cerebral edema
Too rapid rise in sodium indicate cerebral edema result of loss of free water in the urine from DI ,is a sign of cerebral herniation

71. Risk factors of cerebral edema
age<5 yr of age
More severe acidosis at presentation
low pCO2
High blood urea nitrogen
New onset diabetes
Bicarbonate treatment for correction of acidosis

72. Risk factors of cerebral edema
Longer duration of symptoms
Greater volumes of fluid given in the first 4 h
Administration of insulin in the first hour of fluid treatment
Early fall in glucose-corrected sodium during therapy
Greater hypocapnia after adjusting for degree of acidosis

73. Management
Give mannitol, 0.5–1 g/kg IV over 10–15 min, and repeat if there is no initial response in 30 min to 2 h
Hypertonic saline 3% 2.5–5 mL/kg over minutes
Move to ICU
Reduce the rate of fluid administration by one-third

74. Management Elevate the head of the bed. Intubation may be necessary
Aggressive hyperventilation (to a pCO2 22 mm Hg] has been associated with poor outcome
cranial CT scan

75. Management Hourly or more frequently as indicated
vital signs heart rate, respiratory rate, blood pressure
Neurological observations
Amount of administered insulin
accurate fluid input (including all oral fluid and output.
Capillary blood glucose concentration should be measured hourly.
serum electrolytes, glucose, blood urea nitrogen, calcium, magnesium, phosphorus, haematocrit, and blood gases should be repeated two to four hourly
Urine ketones until cleared or blood β-hydroxybutyrate concentrations

76. Case 1
6 years old boy with established diabetes mellitus type 1 about 5 days ago. he must be give insulin .
He is 20 kg ,he is in prepubertal
What’s insulin protocol?

77. انسولين بعد از غذا
انسولين پايه
قند خون
صبحانه
ناهار
شام

78. 0.7×20=14 total dose age Unit/kg Target premeal BS Basal insulin
<5 years
25-30
5-12 years
0.7-1
80-150
40-50
12-18 years
1-1.2
70-130
0.7×20=14 total dose

79. Insulin regimen (analogues basal-bolus)
Bolus3iU
Bolus: 2 iU
Basal: 7 iU
Bolus: 2 iU
Insulin in blood
There may be a need for injecting isophane bd, rather than od when using quick acting analogues in a basal bolus regimen 6 7 8 9 10 11 12 1 2 3 4 5
time
Breakfast
Lunch
Evening Meal
Sleep

80. پايان

82. Satisfactory outcomes have been reported using
an alternative simplified method: after an initial
fluid bolus of 20 mL/kg of normal saline, 0.675%
saline (3/4 normal saline, mmol sodium) is
infused at 2–2.5 times the usual maintenance rate
of fluid administration regardless of the degree
of dehydration, and decreased to 1–1.5 times the
maintenance rate after 24 h, or earlier if acidosis
resolved, until urine ketones are negative

83. ubsequentfluid management (deficit replacement)
should be with an isotonic solution (0.9% saline,
Ringer’s lactate or Plasmalyte) for at least 4–6 h

84. (sodium should rise by
0.5 mmol/L for each 1 mmol/L decrease in glucose
concentration)

85. Initial dose SC: 0.3 unit/kg, followed 1 h later by
SC insulin lispro or aspart at 0.1 unit/kg every
hour, or 0.15–0.20 units/kg every 2 h.
◦ If BG falls to <14 mmol/L (250 mg/dL) before
DKA has resolved, reduce SC insulin lispro
or aspart to 0.05 unit/kg per hour to keep
BG≈11 mmol/L (200 mg/dL) until resolution of
DKA.

86. The starting potassium concentration in the
infusate should be 40 mmol/L. Subsequent potassium
replacement therapy should be based on serum
potassium measurements.
◦ If potassium is given with the initial rapid volume
expansion, a concentration of 20 mmol/L should
be used

87. The maximum recommended rate of IV potassium
replacement is usually 0.5 mmol/kg/h.
• If hypokalemia persists despite a maximum rate
of potassium replacement, then the rate of insulin
infusion can be reduced

88. hypophosphatemia Metabolic encephalopathy (irritability, paresthesias,
confusion, seizures, coma); impaired myocardial
contractility and respiratory failure due to
weakness of the diaphragm; muscle dysfunction
with proximal myopathy, dysphagia, and
ileus; rare hematologic effects include hemolysis,
decreased phagocytosis and granulocyte
chemotaxis, defective clot retraction and thrombocytopenia.
Acute hypophosphatemia in a patient
with preexisting severe phosphate depletion can
lead to rhabdomyolysis

89. To prevent rebound hyperglycemia, the first SC
injection should be given 15–30 min (with rapidacting
insulin) or 1–2 h (with regular insulin) before
stopping the insulin infusion to allow sufficient time
for the insulin to be absorbed

90. degree of edema
that develops during DKA correlates with the degree
of dehydration and hyperventilation at presentation,CEREBRAL HYPOPERFUSION
but not with factors related to initial osmolality or
osmotic changes during treatment

91. 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

92. Major criteria
• Altered mentation/fluctuating level of consciousness
• Sustained heart rate deceleration (decrease more
than 20 beats/min) not attributable to improved
intravascular volume or sleep state
• Age-inappropriate incontinence

93. Minor criteria
• Vomiting
• Headache
• Lethargy or not easily arousable
• Diastolic blood pressure >90mmHg
• Age <5 yr

94. The appearance of diabetes insipidus, manifested
by increased urine output with a concomitant marked
increase in the serum sodium concentration, reflecting
loss of free water in the urine, is a sign of cerebral
herniation causing interruption of blood flow to the
pituitary gland

95. Treatment of cerebral edema
• Initiate treatment as soon as the condition is
suspected.
• Reduce the rate of fluid administration by one-third.
• Give mannitol, 0.5–1 g/kg IV over 10–15 min, and
repeat if there is no initial response in 30 min to 2 h
(210–212).
• Hypertonic saline (3%), suggested dose 2.5–5 mL/kg
over 10–15 min, may be used as an alternative to
mannitol, especially if there is no initial response to
mannitol

96. BARAYE HAR 1 MMOL KAHESH GHAND NA 0.5 MMOL AFZAYESH MIYABAD