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

1. Diabetic
ketoacidosis
Presented by :
Yusor jaafar
Supervised by :
Dr.Haider

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. 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

6. 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

7. Insulin

8. Keton body

9. 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

11. 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)

12. 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

13. 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

14. K+ decrease becauseK+ increase because
Inadequate oral intakeAcidosis
EmesisHyper glycemia
Osmotic diuresisProteolysis

15. 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

16. 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

17. 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

18. Lab assessment
•Urine Ketones +
BUN =40
Na=127mmol/l
–pH 7.05
–pCO2 1.8
–pO2 18
–Bicarb 5.2

19. Lab results

20. Diagnosis

22. ABC
Secure the airway and empty the stomach by
continuous nasogastric suction to prevent
pulmonary aspiration, in case there is
deterioration in conscious level.

23. 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.

24. • Perform continuous electrocardiographic
monitoring to assess T-waves for evidence of
hyper- or hypokalemia
• Give oxygen to patients with severe circulatory
impairment or shock

25. • 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)

26. 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

27. Rehydration•for this patient
Normal (0.9%) Saline
Weight =25kg
Maintenance =1600ml
Deficit =25*100=2500ml (sever dehydration
10%)
Requirement = 4100 ml

28. 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

29. • 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.

30. Ringers Lactate

31. Because
• 1)hypotonic saline = increase risk of cerebral
oedema
• 2)cintain k+
• 3)lactate converted to glucose

32. 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

33. 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.

34. 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

35. Electrolytes

36. 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.

37. Bicarbonate

38. Because
• 1)cause intracelluler acidosis
• 2)increase risk of cerebral oedema because
increase sodium leve in plasma
(hypernatremia)
• 3)cause cellular hypoxia and hypokalemia

39. 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

40. Monitoring chart

43. 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)

44. 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

45. • 5)polmunary oedema / ARDS
• 6)acute renal failure
• 7)bowel ischemia / necrosis / fistula formation

46. 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%

47. Pathophysiology
• Osmotic change

49. • CNS hypoperfusion / ischemia
• Po2
• BUN

50. Risk factors
• Epidemiological factors
• Newly diagnosed cases
• Young age: < 5 years old
• Longer duration of symptoms
• Prolonged illness
• Extended history of poor metabolic control

51. • Therapeutic interventions
• Rapid rehydration (> 50cc/ kg in first 4 hrs)
• Bicarbonate therapy for correction of acidosis
• Insulin administration in the first hour of
therapy

52. • 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

53. 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 )

54. 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

55. Minor criteria
• Headache
• Vomiting
• Diastolic blood pressure >90mmhg
• Lethargy
• Age <5years

57. 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

58. 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.

59. • 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).