objectives

ØDefintion and grading of DKA .

Øclinical & laboratory Dx of DKA.
ØHow to manage DKA.
(what are the recent changes ).
ØTo know and avoid complications
of DKA.
Role of Insulin
 The main aim of this presentation is to
vEarly recognize, diagnose and treat
DKA.
vAvoid progression to serious
complications especially cerebral
edema.
vreduce mortality rates among DKA
patients.
 So prevention , prevention
prevention,
ØHigh index of suspicion to diagnose new onset
type1 DM early before they decompensate into
DKA (pitfalls in diagnosis is common).
Ø Education of known type1 DM about DKA,(symptoms)
how serious, how it occur , how to prevent it.
Ketotic
Stress hyperglycemia
hypoglycemia.
Diabetes mellitus.
Alcohol ketosis. Non-ketotic hyperosmolar
,persistent vomiting. state.
Starvation ketosis Impaired glucose tolerance

ketosis Hyperglycemia

DKA

acidosis
Gastroenteritis.
Lactic acidosis.
Uremic acidosis.
Drug induced acidosis .
IEM.
Peripheral Hospital A;
Tender abdomen MCH
Analgesia? pre Shock state
lapratomy? Abdominal tenderness
Family refused. B. Glucose 480mg
Hospital B Ph 7.13
Abd.Pain & unwell. +++glucosuria
Glucose 430 mg. No ketonuria?????
Ph 7.17 Impression: DKA
Transferred to MCH
 20ml/kg 0.9% saline
MCH
Fluid maintenance + 10% Shock
deficit Abdominal
Insulin infusion 0.1 U/kg/ tenderness
hour B. Glucose 480mg
PICU for close monitoring Ph 7.13
8 hours later glucosuria
ph 7.38, glucose normalised No ketonuria
Pain & vomiting (worse) with Impression:
progressive guarding, rigidity. DKA
with No ketonuria.
Is it DKA?
Stress hyperglycaemia due to midgut volvulus
Urgent lapratomy
 PATHOGENESIS
Ketones
Glucose
DKA
is mainly caused by Acidosis
Hyperglycemia insulin
& Glycosuria
deficiency .and
Osmotic increase in CRH Vomiting
Diuresis Fluid & Electrolyte
Depletion.

Renal Hypo perfusion

Impaired Excretion of Glucose,

Ketones & Hydrogen ions
Warning\ IF you miss type1 DM, they will
progress to DKA DEATH
Type1 DM
Thirst(polydepsia).
Frequent urination(polyuria).
Loosing weight.
High blood glucose levels
Constantly feeling tired
Polyphagia with wt. loss.DD?
DKA
Nausea, vomiting,
or abdominal pain
A rapid breathing
(short, deep breaths)
Fruity odor on breath
Drowsness& confusion
COMA
 Natural history of type1 D.M
80 – 90 % destruction of B.Cells(insulin is low or absent)
Key to
Polydepsia & polyuria
diagnosis

Wt. loss

fatigue

Abdominal pain & vomiting

Acute abdomen

Kussmaul breathing

Disturbed consciousness & coma DEATH

Presentation of DKA
(always preceded by symptoms of diabetes).

ØVomiting .
ØAbdominal pain.
ØFruity odor to breath.
ØDry mouth and tongue & sunken eyes.
ØDrowsiness.
ØDeep breathing.
ØComa.
ØDeath.
 Causes/Precipitating Factors of DKA
üInitial presentation of type 1 diabetes mellitus
üIn a patient with known type 1 diabetes
ØInfusion site problem, tubing problem, or
pump malfunction.
ØIntercurrent illness/infection.
ØMissed insulin injections.
ØStress: psychosocial, trauma, surgery.
Physical Exam;
Determine the grade of DKA
(mild-moderate-sever).
qPerfusion(BP-orthostatic hypotension ,CRT).
qVital Signs - including weight.
qMental Status (baseline GCS)..
qKussmaul breathing.
qDegree of dehydration.
qAcute abdomen and paralytic ileus.
Investigations:
1-Blood tests:
A- blood glucose>200mg/dl.
B-Urea , and serum electrolytes(Na ,K,cl,ca,po4).
C- blood gases(PH<7.3,Hco3<15mEq/l,Po2,Pco2)
D-Blood culture(if febrile & sick to exclude underlying
infection).
2-Urine for :
A-Dipstick for ketonuria and glucosuria(3+or4+).
B-Culture of urine(if UTI is suspected).
3-ECG for hypo. or hyperkalemia.
 At emergency room
qABC , grade DKA , inform Reg. and ICU staff.
qEstablish 2 large intravenous lines for fluids
and insulin infusion,).
q Start N\S 20ml\kg in sever DKA.
1. Check Wight
2. Sent urgent blood sample for:

B.S Na+ Hco3 PH Culture CXR

k+ Urea CBC urine ECG.
& R\E
DLC

AVOID CATHETER start I.V N\S if hypotensive or in shock+O2 in sever cases

 If patient is unconscious
A urinary catheter should be inserted.
qPatients who are unconscious or semi conscious
or have repeated vomiting should have a
nasogastric tube inserted and stomach
emptied. The tube should stay down until the
patient is conscious or vomiting resolved.
 If there is ILEUS at presentation –please don't forget
to decompress the abdomen.

insert a good size nasogastric tube to decompress the abdomen ‘and keep it
open in urine bag ,keep it two feet below patient level.

q ileus ? generalized abdominal tenderness and

distention with sluggish or absent bowel sounds.
Ø WEIGH THE CHILD. If this is not possible because of the
clinical condition, use the most recent clinic weight as a
guideline, or an estimated weight from centile charts. Or
rough estimate depending on age ;
e.g10years=30kg.
 Parameters Mild Moderate Sever

Dehydration 3% 6% >9%
consciousness Alert Alert ∕ drowsy coma
Plasma glucose mg/dl 300 – 400 400 - 600 >600
Peripheral perfusion Normal Normal or decrease ↓↓
Pulse Normal or ↑ Increased Increased
Blood Pressure usually normal Decreased
Normal

PH 7.2-7.3 7.1-7.2 <7.1

ward Icu ICU
Management

Hco3 10-15 5-10 <5

Serum Osmolality:
2[Na+K]+ (glucose/18) + BUN/2.8
normal osmolality?
Serum Na:
Corrected Na =
measured Na + (1.6)(glucose - 100)/100.
Anion Gap:
[Na] – ([Cl]+[HCO3]).
(Normally 12+/-2 mmol/L).
Glucometer& urine dipstick should be available
in ER,ward&ICU(results in seconds).
LAB. MAY TAKE 1hr or two
 Differential diagnosis of DKA:-

1. Acute gastroenteritis( esp. hyper. Na↑ dehydration)

2. Acute abdomen →acute appendicitis.bowel ischemia.

4. Hypoglycemic coma..
5. Pneumonia , bronchial asthma and Hysteria.
6. Salicylate poisoning.. 7- stress Hyperglycemia.

25
In DKA:
ØMortality due to :
-dehydration.
-Hyperkalemia.
-Hypokalemia.
-Hypoglycemia.
-aspiration pneumonia

Is unaccepted
should be prevented , predicted ,
detected early and Rx.
Misleading features in DKA
Ø Signs of dehydration may be overlooked >> hyperosmolarity.
Ø Acute abdomen >> May mimic surgical causes.
Ø Acidotic breathing >> confused with
pneumonia ,asthma or hysteria.
Ø WBC raised >> in absence of infection.
Ø Sodium >> may be falsely low.
Ø N or High Potassium initially >> total K is low.
Ø Urinary ketone check >> not parelling clinical recovery.
Ø S. amylase may be >> in absence of pancreatitis.
Urine testing during DKA
Ø When the clinical condition improves with treatment ,
the urine test results become positive due to the
returning predominance of acetoacetate .
Ø So, during follow up of patients with DKA urine test
for ketones is better avoided.
Ø Now blood ketone measurements are available
and detect beta-HB.(bed-side ketometer).
BSPED Recommended DKA
Guidelines 2009

ØAlways consult with a more senior doctor

on call as soon as you suspect DKA even if
you feel confident of your management.
ØRemember : children can die from
DKA.
The following changes have been
made since the last version (2009)
q 1. Recommendation to use capillary blood ketone
measurement during treatment.

q2. Reduction in the degree of dehydration to be

used to calculate fluids. (4-8%).

q3. Reduction in maintenance fluid rates .

q 4. Change in the recommendations for PICU/HDU – more
emphasis on safe nursing on general wards.
 cont,.
q5. Continuation of Normal saline for the first
12 hours of rehydration.
q6. Delay in insulin until fluids have been running
for an hour.
q7. Option to continue insulin glargine during treatment.

q8. Reminder to stop insulin pump therapy during

treatment.
cont,.
q9. Reminder to consider anticoagulant
prophylaxis in young children, especially
those with femoral lines.

q10. Interpretation of blood ketone

measurements if pH not improving.

q11. Option to use hypertonic saline 2.9%

instead of mannitol for the treatment of
cerebral oedema.
 Confirm the Diagnosis
Ø History : polydepsia , polyuria ,vomiting , abdominal pain
Ø Clinical : acidotic respiration ,acetone smell.
Ø dehydration .
Ø drowsiness .stupor , coma.
Ø abdominal tenderness, ileus.
q Biochemical :
high blood glucose on finger-prick test
(>11 mmol/l)200mg\dl.
Ø blood pH<7.3 and/or HCO3 <15 mmol/l
Ø finger-prick blood ketones >3.0 mmol/l
Ø glucose and ketones in urine.
 FULL CLINICAL ASSESSMENT
Degree of Dehydration in DKA;-
Mild 3% - just clinically detectable (no bolus).
Moderate 3-6% -dry mm , reduced skin turgor, (5-10cc\kg
normal saline over one hour)
Severe 8%-as above with sunken eyes, poor capillary return
(N\S 10\kg-30-60minutes).
+ shock severely ill with poor perfusion, thready
rapid pulse (iv N\S 20\kg\ as fast as possible , you
may need to repeat bolus till perfusion and BP
normalized, max-3 times?

NB reduced BP is not likely and is a very late sign .

 Goals of treatment:
ØRestore perfusion,restore GFR , which will increase
glucose loss in urine,, and decreases the progressive
acidosis.
ØStop ketogenesis by giving insulin, which will
reverse proteolysis and lipolysis, and stimulate glucose
uptake and processing, normalize blood glucose, and
reverse acidosis.
ØCorrect electrolyte (mainly K,Na).
ØAvoid the complications of treatment as possible,
including intracerebral complications
(Cerebral oedema), hypoglycemia, andhypokalemia
 GENERAL
MANAGEMENT; (ABC)

Ø1- CIRCULATORY ASSESMENT:

USUALLY 4-8% DEHYDRATION
Ø2- NEUROLOGICAL ASSESMENTS.
Ø3- ECG MONITORING.
Ø4- ESTIMATE { INPUT & OUTPUT }.
Ø5- RAPID CHECK OF { B.S & BUN & S. ELECTOLYTES
KETONURIA.} { B.GAS 4 HOURLY }
Ø6- NPO.(?NGT open drain if abdomen is distended).
Ø7- DKA fluid sheet.
DKA develops slowly and
should be reversed slowly.
Remind
qDKA typically involves deterioration during
several days, with advancing polyuria and
polydepsia.
qWeakness, lethargy, nausea, vomiting ,
anorexia and the classic periumbilical
abdominal pain.
qDKA protocol and guidelines- (means)
moderate and sever DKA.
Treatment of DKA

qResolving hyperglycemia alone is not

the end point of therapy(it comes
earlier).
üNeed resolution of the metabolic
acidosis and inhibition of ketoacid
production to signify resolution of
DKA.
Your enemy is acidosis not
hyperglycemia. 39
 LR NS

pH 6.0-7.5 4.5-7.0

Na+ 130 154

K+ 0
4
Ca++ 3 0

Cl- 109 154

Lactate 28 0

Calorie 9 0

Osmolarity 273 308

 Treatment – basic rules

MILD DKA mild dehydration , no GIT symptoms

pH 7.25-7.35

can be treated as out pt if parents are educated .?

OR in the ward;
clear fluids , Extra insulin ( Regular) (correction
dose+ RI before meals). OR one and half
maintenance with 20 mmol kcl as 1\2 N\S with D5.
+RGULA insulin SC 0.15-0.3 units\kg\ dose 6hrly).
Depends on (age , duration of diabetes).
 Subcutaneous Insulin correcting Dosing.
BOLUS INSULIN
Units Units BASAL TOTAL TARGET AGE (YR)
Added per Added per INSULIN, % DAILY GLUCOSE
15 g at Meal 100 mg/dL OF TOTAL INSULIN (MG/DL)
above DAILY (U/KG/D)
Target DOSE
0.5 25 – 30 0.6 - 0.7 100-200 0-5
0.5

0.75 40 – 50 0.7 – 1 80-150 5-12

0.75

1-2 40 – 50 1 – 1.2 80-150 12-18

1-1.5
MANAGEMENT OF DKA
MODERATE;

pH 7.1- 7.25 Fully conscious

moderate dehydration
Admit to ICU for slow correction i.v fluids i.v
insulin.

SEVER;
PH < 7.1 , severely dehydrated, disturbed
consciousness.
admit to ICU.,,,, DKA Protocol.
Excessive Free Water

ØCorrected Na =
Na(measured)+1.6 (glucose-100)/100

ØCalculated sodium is low and falling

in many cases of cerebral edema.
 Sever DKA
Ø Only if shocked (poor PP , poor capillary filling with
tachycardia, and/or hypotension) give 20 ml/kg NS
as a bolus, and repeat as necessary,
(if not responding after 2nd bolus?
ØThere is no evidence to support the use of
colloids or other volume expanders in
preference to crystalloids.
 EMERGENCY MANAGEMENT

ØGeneral Resuscitation : A, B, C.
Ø Airway Ensure that the airway is patent and if the
child is comatose, insert an airway.
ØIf consciousness reduced or child has recurrent
vomiting, insert N/G tube, aspirate and leave on
open drainage.
ØBreathing Give 100% oxygen by face-mask.
Ø Circulation Insert two IV cannulae and take blood
samples .
Ø Cardiac monitor for T waves (peaked in hyperkalaemia).
Consider PICU or HDU for the following, and discuss
with a PICU consultant

severe acidosis pH<7.1 with marked

hyperventilation .

 severe dehydration with shock .

 depressed sensorium with risk of aspiration from

vomiting .

under 2 years.

Past H/O cerebral edema.

 Observations to be carried out

Ø strict fluid balance (urinary catheterisation may

be required in young/sick children).

Øhourly capillary blood glucose measurements

Ø capillary blood ketone levels every 1-2 hours

(if available).
Observations to be carried out
Ø headache, or slowing of pulse rate, or any
change in either conscious level or behavior.

Ø any changes in the ECG trace, especially T

wave changes suggesting hyper- or
hypokalaemia.

Ø record all results and clinical signs on a flow

chart.
 1. FLUIDS:
The volume of fluid to be replaced is based on the deficit

(degree of dehydration) plus the maintenance.

for 48 hours, subtract the amount already given as resuscitation fluid and give
the total volume evenly over the next 48 hours.
•Hourly rate = 48 hr maintenance + deficit – resus fluid already given
48
• 0.9% saline is used at the start of IV therapy until blood glucose falls to
14mmol/l(250mg\dl)..
•Once the blood glucose falls to 14mmol/l, add glucose to the fluid(N\S with
D5+K).for the first 12hrs then shift to 0.45%N\S+D5+K,,till the end of IV therapy.
.
FLUIDS
(the new recommendation)
Ø Requirement = Maintenance + Deficit – fluid already given
Ø Deficit (litres) = % dehydration x body weight (kg) .
Ø For most children, use 5% to 8% dehydration to calculate fluids.
Ø Maintenance requirements:
q Weight -
0 – 12.9 kg- 80 ml/kg/24 hrs.
o 13 – 19.9 kg - 65 ml/kg/24 hrs.
o 20 – 34.9 kg- 55 ml/kg/24 hrs.
o 35 – 59.9 kg- 45 ml/kg/24 hrs.
o (>60 kg)- 35 ml/kg/24 hrs.
Ø N.B. Neonatal DKA will require special consideration and larger volumes
of fluid may be required, usually 100-150 ml/kg/24 hours)
Fluid management

q Add calculated maintenance (for 48 hrs) and

estimated deficit, subtract the amount already
given as resuscitation fluid, and give the total
volume evenly over the next 48 hours.
 Fluid management

Hourly rate = 48 hr maintenance + deficit – resusfluid already given

48
Type of fluid(after the 1st hr.)
Ø Initially use 0.9% saline with 20 mmol KCl in 500 ml,
and continue this sodium concentration for at least
12 hours. (latest NICE guidelines).
Ø Once the BG has fallen to 14 mmol/l ( 250 mg /dl ) add
glucose to the fluid.
Ø A bag of 500 ml 0.9% saline with 5% glucose and 30 mmol
KCl should be available from Pharmacy ( If not, make up a
solution as follows - withdraw 50ml 0.9% sodium
chloride/KCl from 500ml bag, and add 50ml of 50% glucose
(this makes a solution which is approximately 5% glucose
with 0.9% saline with potassium).
Type of fluid
ØAfter 12 hours, if the plasma sodium level is
stable or increasing, change to 500ml bags of
0.45% saline/5% glucose/30 mmol\L, KCl.

Ø If the corected sodium is falling, continue with Normal

saline (with or without glucose depending on blood
glucose levels). Some have suggested that Corrected
Sodium levels give an indication of the risk of
cerebral oedema.
 Example :
(6yrs old DKA with sever dehydration).
A 20 kg 6 year old boy who is 8% dehydrated, and who
has already had 20ml/kg saline, will require
8 % x 20 kg = 1600 mls deficit.
plus 55ml x 20kg = 1100 mls maintenance each 24
hours
1100 mls (2200cc maintenance over 48hrs).
= 3800 mls.
minus 20kg x 20ml = 400 mls resus fluid=3400cc.
3400 mls over 48 hours = 71 mls/hour.
Do not include continuing urinary losses in the
calculations at this stage.
c) Oral Fluids :
FREE WATER IS CONTRAINDICATED)

 In severe dehydration, impaired consciousness & acidosis

do not allow fluids by mouth. a N/G tube may be necessary
in the case of gastric paresis.

 children with DKA usually are very thirsty,and their mouth

is very dry ,they will ask for water all the time,what to do?

When good clinical improvement occurs before the 48hr

rehydration period is completed, oral intake may proceed
and the need for IV infusions reduced to take account of
the oral intake.
Children with DKA have dry mouth and
always will ask for water . free
water is dangerous , what to do?
 Don't give water(risk of cerebral
edema),if no ice cubes & enforced to
give fluids ORS is safer than water.
 Insulin Therapy for DKA

qIV infusion with basal rate 0.1 U/kg/hr.

qNo initial insulin bolus – it will decrease time to

correction of the glucose, but does not alter the time to
correction of acidosis(SO it is not desirable).

It may decrease the serum osmolality more rapidly than

desirable.

q Ideal glucose decline is about 50-80 mg%/hr.

qContinue insulin until acidosis corrected and

(blood) ketones are cleared.
 INSULIN :1
((only regular or rapid insulins are
used=IV infusion)).
Ø Once rehydration fluids and potassium are running,
blood glucose levels will start to fall. There is some
evidence that cerebral oedema is more likely if
insulin is started early. Therefore DO NOT start
insulin until intravenous fluids have been
running for at least an hour.

Ø Continuous low-dose intravenous infusion is the

preferred method. There is no need for an
initial bolus.
 INSULIN :
( a separate IV line).
Ø Make up a solution of 0.1 unit per ml. of human soluble
insulin (e.g. Actrapid) by adding 50 units (0.5 ml) insulin to
50 ml 0.9% saline in a syringe pump. Or infusion
pump .or 100u(1cc insulin)+100ccN\S.
Ø The solution should then run at 0.1 units/kg/hour
(0.1ml/kg/hour). A 6yrs ,wt 20kg=2ml\hr. when you
need reduction of insulin to 0.05\kg\hr, run insulin
infusion at 1ml\hr.
 INSULIN :4
qIdeally you shoud keep B.G between
(150-250mg\dl )
throughout Rx of DKA.

ideally the blood glucose should decline by

(50-80mg\dl\hr).
INSULIN :
Ø Once the pH is above 7.3, the blood glucose is down to 14
mmol/l(250mg\dl), and a glucose-containing fluid has been
started, consider reducing the insulin infusion rate, but to no less
than 0.05 units/kg/hour.

Ø If the blood glucose rises out of control, or the acidosis is not

improving after 4-6 hours consult senior medical staff and re-
evaluate (, insulin errors? –insufficient fluids ,Spoiled
insulin, wrong insulin? possible sepsis) .
is the two lines are running with good rate ?),
and consider starting the whole protocol again.
Please remember Lantus is available as
bottle and it is clear(confused with R).
 INSULIN :
qFor children who are already on long-acting insulin
(especially Glargine (Lantus)), your local consultant
may want this to continue at the usual dose and
time throughout the DKA treatment, in addition to
the IV insulin infusion, in order to shorten length
of stay after recovery from DKA.
qFor children on continuous subcutaneous insulin
infusion (CSII) pump therapy, stop the pump when
starting DKA treatment.
 Management cont.
q Once the blood glucose level falls to 14mmol/l(250mg\dl),
change the fluid to contain 5% glucose (generally 0.9%
saline with glucose and potassium).
DO NOT reduce the insulin if acidosis is present.
The insulin dose needs to be maintained at ;
0.1 units/kg/hour to switch off ketogenesis.
INSULIN :

qIf the blood glucose falls

more than 100mg\dl\hr,
what you do?
 INSULIN :

q 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 4 mmol/l(80mg\dl), give a
bolus of 2 ml/kg of 10% glucose and increase the
glucose concentration of the infusion.

qIf needed, a solution of 10% glucose with 0.45% saline

can be made up by adding 50ml 50% glucose to a 500
ml bag of 0.45% saline/5% glucose with 20 mmol KCl.
Insulin management once
ketoacidosis resolved
Continue with IV fluids until the child is drinking well and
able to tolerate food. Only change to subcutaneous insulin
once blood ketone levels are below 1.0 mmol/l, although
urinary ketones may not have disappeared completely.
Discontinue the insulin infusion 60 minutes after the first
subcutaneous injection to avoid rebound hyperglycaemia.
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 (discuss with senior staff).
 Sodium
ØCorrected sodium levels should rise as blood glucose
levels fall during treatment.
If they do not, then continue with Normal saline and
do not change to 0.45% saline.
Ø Check U & E's 2 hours after resuscitation is begun and
then at least 4 hourly .
Ø The following solutions should soon be available
from pharmacies:
Ø 500ml bag of 0.45% saline / 5% glucose containing 20
mmol KCl.
Ø 500ml bag of 0.9% saline / 5% glucose containing 20
mmol KCl.
SODIUM
HYPONATRAEMIA;
ØThis is often pseudohyponatraemia due to the presence of
hyperlipidaemia. It does not require correction.
Use 0.9% saline for the 1st 12hrs.
ØIf sodium is not returning to normal with treatment fluid
replacement needs to be reassessed, as ongoing low sodium or
falling sodium may herald the onset of cerebral oedema.
HYPERNATRAEMIA;
If the serum sodium concentration on rehydration
rises above 150mmols/l the normal saline
infusion should be changed to half normal saline.
Diabetic Ketoacidosis
Treatment - goals Treatment - goals
Total body potassium depletion
in DKA
Loss equals 5-10 mEq / kg body weight.
q Plasma concentrations may be normal or
elevated at time of presentation of DKA.
Ø Water and K are shifted from intracellular to
extracellular space.
Ø Acidosis also causes potassium shift.
Ø Lack of insulin (a promoter of K uptake).
q Secondary hyperaldosteronism can increase
potassium loss.
potassium
The initial serum level is often normal or elevated.
No k the 1st hour..
Once the child has been resuscitated, potassium should be
commenced immediately with rehydration fluid unless anuria is
suspected.
Therefore ensure that every 500 ml bag of fluid
contains 20 mmol KCl (40 mmol per litre).
K level must be closely monitored by ECG until DKA is
substantially resolved.
Parentral K should be started once serum K is normal or
decreased.( 30-40mEq/L).
Its recommended to use K phosphate rather than KCL as K
source( K acetate is also used).
 Diabetic Ketoacidosis
Treatment – Potassium therapy
When you start potassium therapy make sure
Patient is making urine.
Serum potassium is less than 5.5 mmol\L.
Potassium replacement;
20 to 40 mEq per L of IV fluid.
1\2 K acetate, 1/2 KP04 to replace phosphorus.
(ideal but NA). You can use KCL safely.
Patients with severe hypokalemia at admission may
need more aggressive potassium replacement
 May need potassium added to first I.V Fluids &
withhold insulin . till K is >3.5 .
Check potassium level every 1 to 2 hours initially
Kitabchi, A. E., Wall, B. M., Diabetic Ketoacidosis, 1995, Medical Clinics of North America, Vol. 79, 1, pg 17
Potassium ;add K after 1hr of IVF.
qAdd potassium when K<5 and with urination.
ØK >5.5 – no potassium in IVF.
ØK 4.5 – 5.5 – 20 meq/L K+.
ØK <4.5 – 40 meq/L K+.
 Potassium therapy
Treatment – Potassium therapy
q Potassium should not be added to initial first I.V of
saline (0.9%).
Ø Patients are initially hyperkalemic.
Ø Addition of K+ without insulin can cause a dangerous
increase in extracellular potassium & leads to

Ø Cardiac arrhythmias & death.

Kitabchi, A. E., Wall, B. M., Diabetic Ketoacidosis, 2006, Medical Clinics of North America, Vol. 79, 1, pg 17
Management-electrolyte
qPotassium : usually 20-40mEq\l ,and adjust according
to serum potassium level(max 80meq\L)..
qHold insulin if serum potassium is lower than 2.5
mEq/l(o.5-1mmol\kg over 1hr).
qconsider phosphate replacement only if serum
phosphate is lower than 1 mg/dl.
Phosphate
Phosphate deficit is unclear to contribute
to symptoms of DKA such as :-
muscle weakness.
Respiratory depression .
hemolytic anemia .
cardiac dysfunction.
In pediatric patients with DKA it has
not been shown to be of clinical significance.
 BICARBONATE therapy in DKA

qThis is rarely, if ever, necessary.

Continuing acidosis usually means
insufficient resuscitation or insufficient
insulin.
Bicarbonate should only be considered in
children who are profoundly acidotic
(pH< 6.9) and shocked with circulatory
failure. Its only purpose is to improve cardiac
contractility in severe shock.
Bicarbonate: risks!
Ø Rapid correction of acidosis shifts the Hb*O2
dissociation curve to the left, resulting in
impaired tissue oxygen delivery
Ø Rapid correction of the acidosis, with subsequent
movement of potassium intracellularly may result in
hypokalemia
Ø Bicarbonate use has been associated
increased risk of cerebral odema.
Ø Correction of acidosis may result in a
paradoxical CNS acidosis.
ANTICOAGULANT PROPHYLAXIS
qThere is a significant risk of femoral vein thrombosis
in young and very sick children with DKA who have
femoral lines inserted. Therefore consideration should
be given to anticoagulating these children with 100
units/kg/day as a single daily dose of Fragmin.
qChildren who are significantly hyperosmolar might
also require anticoagulant prophylaxis (discuss with
your local consultant).
DKA coagulation changes;

↑ Platellet aggregation.

↑ Level of Von Willibrand factor.

↓ Levels of protein S & C .

 If acidosis is not correcting,
consider the following
q insufficient insulin to switch off ketones .

qinadequate resuscitation.

q sepsis .
q hyperchloraemic acidosis.

q salicylate or other prescription or other drugs

(deliberate\ suicidal).
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Cerebral edema
ØThis is unpredictable, occurs more
frequently in younger children and newly
diagnosed diabetes and has a mortality of
around 25%.

ØThe causes are not known, but this protocol aims

to minimize the risk by producing a slow
correction of the metabolic abnormalities.
 N.B-Please remember;
mild cerebral
oedema on C.T
scan occurs in all
patients with DKA.
 Symptoms and signs of cerebral edema

ØHeadache.
ØD e c r e a s e d o r w o r s e n i n g l e v e l o f
consciousness.
ØSlowing of the HR .
ØIncrease in BP.
ØSudden onset/return of vomiting.
ØWarning signs occur before the onset of CE .
 Clinical Factors Associated with Cerebral
Edema
ØProlonged Illness.
ØSevere acidosis - low PA CO2.
ØSevere dehydration.
ØBicarbonate therapy.
ØPersistent hyponatremia.
ØExcessive fluid admistration.
ØRapid hydration.
ØDiluted fluid admistration.
 Cerebral edema risk factors cont.
ØYounger children (< 4 yrs)
ØInsulin given before fluids.
Etiology of CE
 The exact etiology and mechanism
is not known.

Odmogenic osmoles theory?

It is still a mestery.
Cerebral edema in DKA

Ø This complication of DKA is almost exclusive

condition of childhood.

Ø Comprise the most serious potentially lethal

complication of DKA.
Ø It occurs in 0.3-1% of DKA treated patients.

Ø It usually occurs after 4-12hrs of initiating Rx while

clinical & biochemical parameters are improving.

Ø C.O causes an increase in the volume of the cerebral

content within a rigid cranial cavity.

qHeadache.

qVomiting.

qAltered mental status :

[Sleepiness , Drowsy , confusion , irritability ,

stupor ,Coma ]

q Cushing triad → Hypertension – Bradycardia and

irregular respiration
q Palpilledema ( late sign ).
q Sequent → ptosis and anisocoria due to VI & III
nerve palsies.

q Herniation :
Coma is followed by decorticate rigidity small pupils
and chyne–stokes breathing .
C.T scan:

to establish diagnosis and role out important complication i.e;

cerebral sinus thrombosis (anticoagulant Rx indicated)

DKA ↑ Platellet aggregation.

↑ Level of Von Willibrand factor.

↓ Levels of protein S & C .

Treatment of cerebral edema

ØMannitol: 1 gram/ kg IV over 15-20 minutes.

ØElevate the head of the bed.
ØDecrease IVF rate and insulin infusion rate.
ØPediatric ICU management.
ØDo not delay treatment until radiographic
evidence.
Management :

ØIf CO is suspected inform senior staff immediately.

Øexclude hypoglycaemia as a possible cause
of any behavior changes.
Ø give hypertonic (2.9%) saline (5mls/kg over 5-10
mins) or Mannitol 0.5 – 1.0 g/kg over 10-15 min.
This needs to be given as soon as possible if warning
signs occur (e.g headache or pulse slowing).
Ø restrict IV fluids to 1/2 maintenance and
replace deficit over 72 rather than 48 hours.
Management of C.O:

qIf headache alone.

qFor decreasing level of consciousness.

qIf GCS < 10.

For headache alone

1. Elevate the head of the bed to 30 degree & maintain

in midline.

2. Decrease fluids to maintenance.

3. Closely monitor GCS & Serum Na.

4. Severe headache is an indication of Mannitol

therapy.
For decreasing level of
consciousness

1. As for headache plus.

2. O2 by mask.
3. Mannitol 0.5 – 1 gm/kg
[ 20% solution ] over 10 –15 minutes ,
can be repeated.(or 2.7% saline 5ml\kg
over 5-10 minutes).
 If GCS < 10
Ø As above plus .

Ø Decrease I.V.F to ½ maintenance.

Hyperventilation with bag and mask.

Ø induction of anaesthesia with Lidocain I.V before

intubation

Ø keep PCO2 25 - 35 mmHg.

Ø Correct hyperosmolarity over 72hrs.

1. Suspect diabeteses and DKA in every child who present
with :
 Polyuria and polydepsia.
 Unexplained Wt loss with polyphagia or anorexia.
 Persistent vomiting and abdominal Pain.
 Acute abdomen.
Dehydrated child without diarrhea.
Unexplained tachypnea .

Disturbed consciousness or coma.

2. For children who presented with
moderat to sever DKA :

a). Rehydrated over 48 hrs.

b). Use N\S for the 1st 12hrs,then shift to N\S with
D5 when B.S ↓300 mg / dl .after 12 hrs check
corrected Na and decide.
c). Don’t give more than 4L/m2/24hrs of

fluid (and don’t give more than 8% deficit)

d). Don’t use NaHCO3 to Rx acidosis.
a) Don't start insulin before the 1st hour .
b). Don't forget to start potassium when you
start insulin infusion.
c). Don't discontinue insulin if sugar is low
and patient still acidotic, give dextrose
bolus and increase sugar concentration.

d) Don't use 1\5 DS, at any stage of DKA

management unless 1\2NS is not available.
3- Suspect C.O if :

a. Disturbed consciousness at presentation is not

improving or getting worse.

b. Development of Headache and vomiting. And

deteriorating mental status after apparent
improvement between 3-24hrs after starting
therapy.

c. if you suspect C.O start management and

arrange for C.T scan ( Don’t delay Rx ).
Thank you