1. IN THE NAME OF GOD

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

3. Case study
کودک 6 ساله ای با وزن 20 کیلو گرم با تنفس تند به اورژانس وارد شده
در بدو ورود
تصمیم 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. Fluid therapy
Maintenance
Deficit
Abnormal ongoing loss

21. 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.

22. Fluid therapy 1-within first 12 hours ½Deficit +½ Maintenance
2- within next 12 hours
1̸ 4Deficit + ½ Maintenance
To replace the estimated fluid deficit evenly
Over h.
ISPAD clinical practice consensus guidelines 2014

23. First Method WT=20kg Maintenance =1500cc Deficit =100 *20 2000cc
مایع 12 ساعت اول =1750
مایع 12ساعت بعدی =1250
در واقع در 12 ساعت دوم و سوم بیمار هر بارcc 1250 مایع دریافت می کند

24. Second Method Iv rate= 85cc/kg+maintenance- bolus÷ 23hr
Iv rate= 85* ÷ 23hr
Iv rate= 126 cc /hr
Nelson 2014

25. Third Method First day 1.5-2 times the 24 h maintenance requirements
10- 20ml · kg-1 · h
with isotonic solution 0.9% saline,Ringer’s lactate for at least 4–6 h
Then half salin 0.45% salin
The second day times the 24 h maintenance requirements
Pediatric Diabetes 2014
ISPAD clinical practice consensus guidelines 2014

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

27. 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

28. Volume Expansion
10-20 ml/kg NS within minutes

29. Volume Expansion Repeated 10ml/kg if Shock Hypotension
Delay capillary refilling
Decrease tissue perfusion

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

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

32. مایع 6 ساعت بعدی
126*6 = 756 cc
دکستروز5% همراه با 75 میلی اکی والان درلیتر سدیم
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

33. 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

34. Fluid therapy Acidosis with BS 100-200mg/dl
Add%7.5 dextrose to solution
Insulin should be continue

35. Fluid therapy Acidosis with BS <100mg/dl
Add%10 dextrose to solution
Insulin should be continue

36. Fluid therapy .
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

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

38. Fluid therapy NS with added potassium was used after urination
Pediatr Crit Care Med 2004 Vol. 5, No. 5

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

40. Potassium K=3-4 40mEq/l K=4-5 20mEq/l
k<3mEq/l insulin should be hold temporary
Give mmol/kg/h iv and oral
Endocrinol Metab Clin N Am 35 (2006) 725–751

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

42. Bicarbonate Therapy After 2-3hours of hydration if
pH <7.0 or bicarbonate <5 mEq
Give 1meq/kg over 1 hour

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

44. 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

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

46. WARNING SIGNS BG falls >90 mg/dL/hour Headache Slowing heart rate
Irritability
Decreased conscious level
incontinence
specific neurological signs
Hypoglycemia

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

48. Insulin therapy
The administration of insulin without fluid replacement in such patients with hypotension may aggrevate hypotension

49. درمان با انسولين روش اول– مداوم
ابتدا در cc100 نرمال سالين ، 10 واحد انسولين كريستال مي ريزيم و براي بيمار 0.1iu/kg انسولين شروع مي كنيم تا قند خون به 300 برسد. پس از آن درمان به طريق زیررا بر اساس درجه اسيدوز با يكي از دو روش ذيل ادامه مي دهيم
اگر اسيدوز باقي باشد دوز انسولين را با نصف ادامه مي دهيم
اگر اسيدوز بر طرف شده باشد ، انسولين مداوم قطح مي گردد.

50. 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

51. DKA management with SC &IM insulin
Initial dose SC: 0.3 unit/kg,
Followed SC insulin lispro or aspart 0.20 units/kg every 2 h.
if BG falls to <250 mg/dL before DKA has resolved Reduce SC insulin lispro or aspart to 0.05 unit/kg per hour
To keep BG200 mg/dL until resolution ofDKA.

52. انسولين درماني
Mild to moderate DKA1-در صورتي که هر 4-3 ساعت زير جلدي تزريق مي کنيم0.25IU/KG انسولين کريستال

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

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

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

56. پس از خروج از کتواسیدوزیس چه می کنید ؟
0.25iu/kg انسولین کریستال هر 4-6 ساعت می دهیم

57. 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

58. Warning signs and symptoms of cerebral edema
Change in neurological status
specific neurological signs (cranial nerve palsies)
Headache
Decreased oxygen saturation
Recurrence of vomiting
Blood glucose falls > (90 mg//hour

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

60. 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

61. 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

62. 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

63. 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 10–15 min
Restrict IV fluids by one-third
Move to ICU
Consider cranial imaging

64. پايان

66. Amount of administered insulin.
• Hourly (or more frequently as indicated) accurate
fluid input(including all oral fluid)and output.
• Capillary blood glucoseconcentration should be
measured hourly

67. Laboratory tests: serum electrolytes, glucose, blood
urea nitrogen, calcium, magnesium, phosphorus,
hematocrit, and blood gases should be repeated
2–4 h, or more frequently, as clinically indicated,
in more severe cases.
• Blood BOHB concentrations, if available, every 2 h

68. The objectives of fluid and electrolyte replacement
therapy are:
• 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

69. he objectives of fluid and electrolyte replacement
therapy are:
• 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 bloo

70. 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

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

72. infuse fluid each day at
a rate that seldom exceeds 1.5–2 times the usual
daily maintenance requirement

73. Start insulin infusion 1–2 h after starting fluid
replacement therapy; i.e., after the patient has
received initial volume expansion

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

75. If BG falls very rapidly (>5 mmol/L/h) after initial
fluid expansion, consider adding glucose even
before plasma glucose has decreased to 17 mmol/L
(300 mg/dL).

76. 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.

77. 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

78. 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

79. 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

80. 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

81. 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

82. Disruption
of the blood–brain-barrier has been found in cases
of fatal cerebral edema associated with DKA (196,
197), which further supports the view that cerebral
edema is not simply caused by a reduction in serum
osmolality

83. increased risk of cerebral edema include
Younger age (198)
• New onset diabetes (170, 198)
• Longer duration of symptoms
or an early fall in glucose-corrected sodium during
therapy (83–85, 202).
• Greater volumes of fluid given in the first 4 h (88,
200, 202).
• Administration of insulin in the first hour of fluid
treatment

84. Greater hypocapnia at presentation after adjusting
for degree of acidosis (85, 183, 200).
• Increased serum urea nitrogen at presentation (85,
183).
• More severe acidosis at presentation (88, 201, 202).
• Bicarbonate treatment for correction of acidosis (85,
203).
• A marked early decrease in serum effective
osmolality (99, 202).
• An attenuated rise in serum sodium concentration

85. 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

86. WARNING SIGNS:
blood glucose falls >5 mmol/l/hour (90 mg/d L) headache, slowing heart rate,
irritability, decreased
conscious level, incontinence,
specific neurological signs
Exclude hypoglycaemia
Is it cerebral edema

87. Management
Give mannitol g/kg or
hypertonic saline
Restrict IV fluids by one-third
Call senior staff
Move to ICU
Consider cranial imaging
only after patient stabilised

88. 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

89. 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

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

91. 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

92. 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

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