4. 4
✓DKA occurs in 20-40% of children with new-onset
diabetes
✓Risk of DKA in Type 1 diabetes is 1% -10% per patient
per year
✓Risk is increased in children with known diabeteswho
omit insulin doses or who do not successfully manage
an intercurrent illness
6. 6
The biochemical criteria for the diagnosis :
❖ Hyperglycemia (blood glucose >11 mmol/L [200 mg/dL])
❖ Venous pH <7.3 or serum bicarbonate <18 mmol/L
❖ Ketonemia (blood b-hydroxybutyrate >3mmol/l) or moderate or
large ketonuria.
✓DKA is the end result of the metabolic abnormalities resulting
from a severe deficiency of insulin or insulin effectiveness
✓The latter occurs during stress as counterregulatory hormones
block insulin action.
9. 9
✓ Dehydration
✓ Tachypnea; deep, sighing (Kussmaul) respiration
✓ Nausea, vomiting, and abdominal pain that may mimic
an acute abdominal condition
✓ Confusion, drowsiness
✓ Loss of consciousness
11. 11
✓Acidosis - Blood pH < 7.3 or
Plasma bicarbonate <18 mmol/litre
✓Ketonemia - blood beta-hydroxybutyrate >3 mmol/litre
✓Urinary ketones of >2+ on standard dipsticks are
equivalent to near patient blood ketones of >3.0 mmol/l.
✓Urinary ketones must be read 15 seconds after stick is
dipped.
15. 15
✓Children with new onset of type 1 diabetes frequently present with DKA
✓Delayed diagnosis of diabetes is an important factor increasing the risk
of DKA and this association has been particularly evident in SARS-CoV2
pandemic
✓In children with established diabetes, the risk of recurrent DKA is 1-10%
per patient per year
✓Most cases are due to insulin omission or interrution of insulin delivery
in patients
19. 19
GENERALRESUSCITATION:A, B, C
✓ Airway : Ensure airway patency
✓ If child has recurrent vomiting, consider inserting NG tube .
✓ Breathing : Give 100% oxygen by face-mask.
✓ Circulation : Measure blood pressure and heart rate
20. 20
INITIAL FLUID BOLUS
In Patients with shock
➢Shock is defined by the (APLS definition ) presence of tachycardia,
prolonged CRT, poor peripheral pulses and hypotension
➢they require appropriate restoration of their circulation and
circulatory volume.
➢They should receive a 10 ml/kg bolus over 15 minutes.
21. 21
✓ For the initial treatment of shock- consider isotonic
crystalloids (eg Plasmalyte 148 or Ringers lactate) .
✓ 0.9% Saline is used if these are not available.
✓ Following the initial 10 ml/kg bolus they should be
reassessed and further boluses of 10 ml/kg may be given if
required.
✓ To restore adequate circulation bolus can be given up to a
total of 40 ml/kg later which inotropes should be
considered.
22. 22
✓ It is important to ensure that the circulation is adequate and
avoid excessive fluid for the risk of cerebral edema
✓Cerebral perfusion is dependant on both perfusion pressure
and intracranial pressure.
✓ Hypotension will exacerbate the risk of brain injury.
23. 23
Patientsnot in shock
✓ All children and young people with mild, moderate
or severe DKA who are not in shock are given 10
ml/kg 0.9% sodium chloride bolus over 30 minutes.
24. 24
INITIAL INVESTIGATIONS
✓ Blood glucose
✓ CBP, Urea and electrolytes
✓ Blood gases (venous or capillary)
✓ Ketones - Near patient blood ketones (beta-hydroxybutyrate) testing .
25. 25
✓ Other investigations are done if needed e.g. CXR, CSF,
throat swab, blood cultures, urinalysis, culture and
sensitivity etc.
✓ A raised WBC count is common in DKA and does not
necessarily indicate sepsis.
✓ DKA may be precipitated by sepsis or intercurrent infection.
✓ Infection may co-exist with DKA.
✓ Suspect sepsis if there is fever or hypothermia,
hypotension, refractory acidosis or lactic acidosis.
✓ A high lactate should increase concern about possible
infection or sepsis.
27. 27
1. Conscious Level - Institute hourly neurological observations
including Glasgow Coma Score whether or not drowsy on
admission
2. Full Examination - looking particularly for evidence of cerebral
oedema headache, irritability, slowing pulse, rising blood pressure,
reducing conscious level ,papilloedema is a late sign
-Infection
-Ileus (which is common in DKA)
3. WEIGH THE CHILD
If this is not possible use the most recent clinic weight as a
guideline or an estimated weight from centile charts.
28. 28
FLUIDS
✓ All fluids given should be documented carefully
✓Volume of fluid - By this stage, the circulating volume should have been
restored.
✓ Children with shock should have been adequately resuscitated with
appropriate fluid volume replacement.
✓Other patients with DKA will have received an initial fluid bolus of
10ml/kg as part of the routine management of DKA.
29. 29
✓Once circulating blood volume has been restored and the child
adequately resuscitated, fluid requirement is calculated as
follows:
✓Requirement = Deficit + Maintenance
✓
✓Estimation of the fluid deficit should be based on the initial
blood pH.
✓The fluid deficit should be replaced over 48 hours alongside
maintenance fluids.
31. 31
RESUSCITATION FLUID
✓The fluid boluses given for resuscitation in children with
shock should NOT be subtracted from the estimated fluid
deficit.
✓The initial 10ml/kg bolus given to all patients not in shock
requiring IV fluids SHOULD be subtracted from total calculated
fluid deficit.
32. 32
MAINTENANCEFLUID
✓Maintenance fluid volumes should be calculated using the Holliday-Segar
formula
✓Maintenance Fluid:
- 100 ml/kg/day for the first 10 kg of body weight
- 50 ml/kg/day for the next 10 to 20 kg
- 20 ml/kg/day for each additional kilogram above 20 kg
33. 33
FLUID CALCULATION
✓ Calculate the fluid deficit (either 5% or 10% dehydration depending on
whether the patient has mild, moderate or severe DKA),
✓ Subtract the initial 10ml/kg bolus (unless given for Shock) then divide this
over 48 hours and add to the hourly rate of maintenance fluid volume
✓ Give the total volume evenly over the next 48 hours
✓ i.e. Weight Hourly rate = ({Deficit – initial bolus} / 48hr) + Maintenance per
hour
34. 34
WEIGHT
✓Whenever possible the patient’s actual weight on admission should
be used rather than an estimated weight or approximation.
✓ Maintenance fluids should be based on the actual weight not an
estimate of the likely weight following rehydration.
✓To avoid excessive amounts of fluid in overweight and obese
children it is recommended that consideration be given to using a
maximum weight of 75kg or 97th centile weight for age (whichever is
lower) when calculating both deficit and maintenance requirements.
37. 37
TYPE OF FLUID
✓0.9% sodium chloride with 20 mmol potassium chloride in 500 ml (40
mmol per litre) is used until blood glucose levels are less than 14
mmol/l (250mg/dl).
✓Plasmalyte148 has been suggested as an alternative as it has a
lower chloride content and therefore hyperchloremic acidosis is less
likely.
✓NOTE: Additional potassium need to be added to Plasmalyte 148 as
it only contains 5mmol/l Potassium.
38. 38
ORAL FLUIDS
✓ Do not give oral fluids to a child or young person who is
receiving intravenous fluids for DKA until ketosis is resolving
and there is no nausea of vomiting.
✓ A nasogastric tube may be necessary in the case of gastric
paresis
✓ If oral fluids are given before the 48hr rehydration period is
completed, the IV infusion needs to be reduced to take account
of the oral intake.
39. 39
BSPED GUIDELINES
Emergency management :
✓Patients in shock :10ml/kg bolus given over 15 min and can be
repeated upto 40ml/kg
✓Patients not in shock : 10ml/kg bolus given over 30 min
Fluid replacement :
✓Deficit : corrected in 48 hrs
✓5% and 7% dehydration respectively for mild and moderate DKA
✓10% dehydration for severe DKA
Maintenance fluid:
✓100 ml/kg/day for the first 10 kg of body weight
✓ 50 ml/kg/day for the next 10 to 20 kg
✓ 20 ml/kg/day for each additional kilogram above 20 kg
40. ISPAD GUIDELINES
40
Emergency management
✓Patients in shock:10-20 ml/kg bolus over 30 min
and repeat until circulation restored
✓Patients not in shock :10ml/kg bolus given over 1 hr
Fluid replacement
✓Deficit : corrected in 24-48 hrs
✓5% dehydration if there is prolonged capillary refill
time and abnormal skin turgor
✓10% dehydration if there is presence of weak or
impalpable pulses ,hypotension, oliguria
Maintenance fluid is same as BSPED guidelines
41. 41
FLUID LOSSES
➢If a massive diuresis continues for several hours fluid input
may need to be increased.
➢ However urinary losses should not be routinely replaced.
➢If large volumes of gastric aspirate continue, these will need
to be replaced with 0.45% saline with Potassium Chloride.
42. 42
POTASSIUM
✓Ensure that all fluids (except initial bolus) contain 40 mmol/l KCL , unless
there is evidence of renal failure.
✓Hypokalemia can occur up to 48 hours after starting DKA treatment.
✓ As Potassium is mainly an intracellular ion there is always depletion of
total body potassium although initial plasma levels may be low, normal or
even high.
✓ Levels of potassium will fall once insulin is started.
✓Therefore for every 500 ml bag of fluid add 20 mmol potassium chloride (40
mmol / litre).
43. 43
If Potassium is above the upper limit of normal range at
presentation it is recommended that :
✓To add potassium to I.V fluids after the patient has passed urine
or gives a history of having recently passed urine
✓ Or after the Potassium has fallen to within the upper limit of the
normal range
✓ It is recommended that the Potassium should be less than
5.5mmol/l in such circumstances.
44. 44
✓If Potassium is low at presentation <3.0 mmol/l then insulin
administration should be deferred until Potassium is >3.0mmol/l.
✓ This may require high concentrations of intravenous Potassium in
fluids which would require a central line.
✓When obtaining central access is likely to result in significant delays
to starting Insulin then oral Potassium can be considered following
discussion with an intensivist to correct hypokalemia.
45. 45
INSULIN
✓Once rehydration fluids and potassium are started, blood
glucose levels will start to fall.
✓There is some evidence that cerebral oedema is more likely if
insulin is started early.
✓Intravenous insulin should not be given as a bolus
46. 46
✓Insulin at a rate of 0.05 Units/kg/hr or 0.1 Units/kg/hr are typically
suggested.
✓ But there is no evidence that one dose is superior to the other.
✓An infusion rate of 0.05 Units/kg/hr is sufficient in most cases, and have
a lower incidence of subsequent hypoglycemia
✓ In severe DKA an infusion rate of 0.1 Units/kg/hr may be needed.
✓ It is recommended that a starting dose of 0.05 Units/kg/hr should be used
unless severe DKA or in adolescents.
47. 47
Other insulin management
✓ In children and young people on continuous subcutaneous
insulin infusion (CSII) pump therapy, stop the pump when starting
intravenous insulin.
✓ For children already on long-acting insulin, you may wish to
continue this at the usual dose and time throughout the DKA
treatment, in addition to the IV insulin infusion.
48. 48
BICARBONATE
✓ Intravenous sodium bicarbonate is not recommended to
children and young people with DKA.
✓ Only consider bicarbonate if there is life threatening
hyperkalemia or in severe acidosis with impaired myocardial
contractility.
49. 49
RISK OF VENOUS THROMBOSIS
✓There is a significant risk of femoral vein thrombosis in young and very
sick children with DKA who have femoral lines inserted. Line should be in
situ for as short a time as possible.
✓ Thromboembolic prophylaxis should be considered in young people
>16 years.
✓And in young women taking the combined oral contraceptive pill and
sick patients with femoral lines, following discussion with an Intensive
Care Specialist.
50. 50
MONITORING
❖Strict fluid monitoring using input output charts
❖ Hourly capillary blood glucose measurements
❖ Capillary blood ketone levels every 1-2 hours
❖ Hourly BP and basic observations
❖ Hourly level of consciousness initially, using the
modified Glasgow coma score
51. 51
✓ Half-hourly neurological observations, including level of
consciousness
✓ Heart rate, in children < 2 years and Ph< 7.1 because of
increased cerebral oedema risk
✓ Watch for symptoms of headache, slowing of pulse rate, or
any change in conscious level
✓ Reporting any changes in the ECG trace, especially signs of
hypokalemia, including ST-segment depression and
prominent U-waves
✓ Twice daily weight is helpful in assessing fluid balance
52. 52
MEDICAL REVIEWS
At 2 hours after starting treatment, and then at least every 4
hours, carry out and record the results of the following
blood tests –
✓ Glucose (laboratory measurement)
✓ Blood gas (for pH and pCO2)
✓ Plasma U&E - ensure samples are sent URGENTLY to lab
✓ Finger-prick (near patient) blood ketones
53. 53
ANION GAP
✓ If the clinical picture is not improving consideration should
be given to calculating the anion gap.
✓ The anion gap is typically 20-30 mmol/l in a patient with
ketoacidosis.
✓ However an anion gap >35 mmol/l may suggest concomitant
lactic acidosis due to sepsis or poor perfusion and should
prompt a review of the overall clinical picture.
✓ It is not required for routine monitoring but may be helpful if
the clinical picture or biochemistry is not improving
54. 54
HYPERCHLOREMIC METABOLIC ACIDOSIS
✓ It may occur following the administration of large amounts of
chloride containing fluids given during the management of
DKA.
✓ The preferential renal excretion of ketones instead of chloride
can result in hyperchloremia.
✓ The acidifying effect of chloride can mask the resolution of
ketoacidosis if base deficit alone is used to monitor progress.
55. 55
✓ Acidosis due to hyperchloremia will correct
spontaneously and doesn’t need specific treatment.
✓ It need not delay the transition to oral fluids and
subcutaneous insulin.
✓ It needs differentiating from ongoing ketosis
56. 56
CRITERIA
❖Plasma Glucose >33.3 mmol/l (600 mg/dl)
❖Arteria PH >7.30
❖Venous PH >7.25
❖Serum Bicarbonate >15 mmol/l
❖Small ketonuria, absent to small ketonemia
❖Effective serum osmolality >320 mOsm/kg
❖Obtundation, combativeness or seizures (in approx.
50% cases)
57. 57
PHOSPHATE AND HYPOPHOSPHATEMIA
✓ Phosphate is lost during DKA due to the osmotic diuresis and
serum phosphate is often low in the recovery phase of severe
DKA.
✓ Supplements or replacement, for example potassium acid
phosphate, are not required unless there is severe hypo
phosphataemia associated with metabolic encephalopathy,
reduced myocardial contractility, myopathy, dysphagia or ileus.
✓ Clinicians should be aware that administration of phosphate
can precipitate hypocalcemia.
59. 59
✓ Continue with 0.9% sodium chloride containing 20 mmol potassium
chloride in 500ml until blood glucose levels have fallen to 14 mmol/l.
✓If the blood glucose rises out of control, or the pH level is not
improving after 4-6 hours
✓Then re-evaluate for possible sepsis, insulin dosage errors, fluid
calculation error or other conditions, and consider starting the whole
protocol again.
✓ If the blood ketone level is not falling within 6–8 hours then consider
increasing the insulin dosage to 0.1 units/kg/hour or greater.
60. 60
Once the blood glucose has fallen to 14 mmol/l add glucose to the fluid
and think about the insulin infusion rate, as follows –
✓ Change the fluid to contain 5% glucose
✓ Use 500 ml bags of 0.9% sodium chloride with 5% glucose and 20 mmol
potassium chloride in 500ml which are available from Pharmacy
✓ Reduce insulin infusion rate to 0.05 units/kg/hr from 0.1 Units/kg/hour
(or maintain at that rate if patient initiated on 0.05 units/kg/hr)
61. 61
✓ If child is on 0.1 units/kg/hour insulin infusion or a higher
dose of insulin then change the fluid to contain 10% glucose
rather than 5% glucose, in order to prevent hypoglycemia
✓ Once ketones are < 1.0 mmol/l, consider switching from
intravenous to subcutaneous insulin
62. 62
✓DO NOT stop the insulin infusion while glucose is being infused, as
insulin is required to switch off ketone production.
✓If the blood glucose falls below 6 mmol/l(18 mg/dl) - increase the
glucose concentration of the intravenous fluid infusion
✓ If there is persisting ketosis, continue to give insulin at a dosage of
least 0.05 units/kg/hour
✓If the blood glucose falls below 4 mmol/l,(72 mg/dl) give a bolus of 2
ml/kg of 10% glucose and increase the glucose concentration of the
infusion.
63. 63
If acidosis is not correcting, consider the following :
❖ Insufficient insulin to switch off ketones (including incorrectly
made insulin infusion)
❖ Inadequate resuscitation
❖ Fluid calculation error
❖ Sepsis
❖ Hyperchloremic acidosis
65. 65
✓Think about stopping intravenous fluid therapy when ketosis is
resolving and oral fluids are tolerated without nausea or vomiting.
✓Do not change from intravenous insulin to subcutaneous insulin until
ketosis is resolving
✓Start subcutaneous insulin at least 30 minutes before stopping
intravenous insulin.
66. 66
✓For a child or young person with DKA who is using insulin pump
therapy, restart the pump at least 60 minutes before stopping
intravenous insulin.
✓ Change the insulin cartridge and infusions set, and insert the cannula
into a new subcutaneous site.
✓Subcutaneous insulin should be started according to local protocols
for the child with newly diagnosed diabetes, or the child should be
started back onto their usual insulin regimen at an appropriate time
68. CEREBRAL OEDEMA
68
Signs and symptoms of cerebral edema include:
✓Onset of headache after beginning treatment or
progressively worsening headache.
✓Change in neurological status (irritability, confusion,
inability to arouse, incontinence).
✓Specific neurological signs (eg, cranial nerve palsies,
papilledema).
✓Cushing's triad (rising blood pressure, bradycardia, and
respiratory depression) is a late but important sign of
increased intracranial pressure.
✓Decreased O2 saturation
69. 69
✓Clinically significant cerebral edema usually
develops within the first 12 hours after treatment has
started
✓ It can occur before treatment has begun or rarely
may develop as late as 24 to 48 hours after the start
of treatment.
✓Although mild to mod headache at presentation
may not be unusual development of a severe
headache after commencing treatment is always
concerning
70. 70
✓ One diagnostic criterion, two major criteria or one
major and two minor criteria have a sensitivity of 92%
and a false positive rate of only 4% to diagnose
cerebral odema
✓Signs that occur before treatment should not be
considered in the diagnosis of cerebral edema
✓ Neuroimaging is not required for diagnosis of
cerebral edema
71. 71
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 (eg, grunting,
tachypnea, Cheyne-Stokes respiration, apneusis)
72. 72
MAJOR CRITERIA
▪ Altered mentation, confusion, 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
73. 73
MINOR CRITERIA
✓ Vomiting
✓ Headache
✓ Lethargy or not easily arousable
✓ Diastolic blood pressure >90 mm Hg
✓ Age< 5 years
74. 74
Treatment of cerebral oedema
Treat the patient immediately for cerebral oedema using
the most readily available of
✓3% hypertonic saline -2.5-5 ml/kg over 10-15 minutes
or
✓ 20% mannitol -0.5-1 g/kg over 10-15 minutes
✓3% Hypertonic saline 2.5 mL/kg is equimolar to
mannitol 0.5 g/kg.
✓In addition fluids should be restricted to ½
maintenance rates
75. 75
✓ The effect of mannitol is within 15 minutes and lasts for
120 minutes.
✓If there is no improvement with mannitol within 30 minutes
a repeated dose of mannitol can be given
✓Mannitol promote a brisk diuresis due to its osmotic effect
and renal excretion.
✓ If mannitol was given initially and there is no response to
mannitol treatment within 15-30 minutes then hypertonic
saline may be also be given
✓ there is some suggestion that the effect of mannitol and
hypertonic saline may be additive.
76. OTHERCOMPLICATIONS
76
✓ Hypoglycemia and hypokalemia – avoid by careful
monitoring and adjustment of infusion rates.
Consideration should be given to adding more glucose
if BG falling quickly even if still above 4 mmol/l.
✓ Systemic Infections – Antibiotics are not given as a
routine unless a severe bacterial infection is
suspected. Fever, raised lactate and raised
inflammatory markers may all indicate possible
concomitant infection.
✓ Aspiration pneumonia – avoid by nasogastric tube in
vomiting child with impaired consciousness
77. 77
MORBIDITY AND MORTALITY
✓In population studies, the mortality rate from DKA in children is 0.15% to
0.30% and may be decreasing.
✓ Recent data show that DKA is still the leading cause of death in subjects
with T1D diagnosed less than 15 years of age
✓ Mortality risk is substantially increased in patients with chronically poor
glycemic control and recurrent DKA.
✓Cerebral injury is the major cause of mortality and morbidity and cerebral
edema accounts for 60% to 90% of all DKA deaths.
78. 78
PREVENTION OF RECURRENT DKA
✓Management of an episode of DKA is not complete until its cause has
been identified and an attempt made to treat it.
✓ Insulin omission, either inadvertently or deliberately, is the cause in most
cases.
✓ The most common cause of DKA in insulin pump users is failure to take
extra insulin with a pen or syringe when hyperglycemia and
hyperketonemia or ketonuria occur.
✓ Home measurement of blood BOHB concentrations, when compared to
urine ketone testing, decreases diabetes-related hospital visits
✓ Blood BOHB measurements may be especially valuable to prevent DKA
in patients who use a pump because interrupted insulin delivery rapidly
leads to ketosis.
79. 79
REFERENCES
❖Nelsons textbook of paediatrics
❖BSPED GUIDELINES (British society for paediatric
endocrinology and diabetes)
❖ISPAD GUIDELINES (International society for
paediatric and adolescent diabetes)
