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Acute Diabetic Ketoacidosis (DKA)

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Diabetic ketoacidosis (DKA) is caused by absolute or relative insulin deficiency and elevated levels of counter-regulatory hormones leading to hyperglycemia, osmotic diuresis, dehydration, lipolysis and acidosis. It is a life-threatening complication of diabetes mellitus that requires prompt treatment.

The basic causes of DKA are absolute or relative insulin deficiency and elevated levels of counter-regulatory or stress hormones like glucagon, cortisol, growth hormone and catecholamines. This leads to increased glucose production and decreased glucose use causing hyperglycemia and subsequent osmotic diuresis, dehydration, lipolysis and acidosis from ketone production.

Common presenting symptoms of DKA include history of polyuria, polydipsia and weight loss. Patients may present with nausea, vomiting, lethargy and fruity breath. Mild cases present alert while severe cases present with drowsiness or coma with possible hyperventilation, dehydration or abdominal pain.

Acute Diabetic Ketoacidosis(DKA)

• Definition:-
DKA can be defined as a blood glucose
level usually >250mg/dl, pH <7.25 & plasma
bicarbonate level of 15mEq/l or less.
Severe DKA is define as a pH of 7.1 or less &
bicarbonate level of 10mEq/l or less.
DKA is a common & potentially life threatening,
acute complication of IDDM. Mortality rate may
be as high as 6-10%.
Pathophysiology

• The basic causes of DKA are absolute or


relative insulin deficiency & elevated levels
of counter-regulatory or stress hormones
(eg.glucagon,cortisol,GH,catecholamines)
that antagonizes insulin. Due to these
hormonal abnormalities, there is increased
glucose production & decrease glucose
use. This causes hyperglycemia, which
leads to an osmotic diuresis, dehydration,
lipolysis, hyperlipidemia.
Cont;
• There is acidosis due the production of
ketones (acetoacetate, B-hydroxybutyate)
from fatty acids. Electrolyte abnormalities
are also present due to intra cellular-
extracellular shifts and urinary losses.
Presentation:
• Usually a patient with DKA presents with H/O
polyuria, polydipsia & weight loss. Acutely pt, is
ketotic & acidotic with fruity breath due to
ketosis. There may be nausea, vomiting &
lethargy.
• Mild DKA pts, may be awake & alert; but in
severe DKA ,pt has drowsiness or coma. There
may be hyperventilation, dehydration or
abdominal pain.
DKA should be suspected in a child who has
vomiting & dehydration but has polyuria.
Precipitating factors
• DKA should be precipitated in a known
diabetic patient by:
An acute infection
Omission of insulin dose.
Approach
• 1)History:-known diabetic? Missed dose of
insulin?
Precipitating factors
Source of infection
H/O wt, loss
2) Physical exam:-
i) level of consciousness:-lethargic/weak;
altered mental state (irritability to deep coma);
sign of head trauma
ii) Vital sign:-pulse (tachycardia, feeble pulse);
temp, (increase or decrease); respiration
(kussmaul’s resp; acidotic odour); BP (normal or
hypertension)
iii) Signs of dehydration:-general condition, pulse,
BP, cap.refilling, skin turger, mucous membrane,
urine output, signs of poor perfusion like cold
clammy extremities.
iv) Systemic exam:- find source of infection if any.
v) Abdominal exam:-may present like acute
abdomen.Look for distention/tenderness/BS
Investigations
i) Blood:- blood glucose(>300mg/dl);urea,
creatinine; Na/K decrease; ketones(+);
pH(<7.3); serum osmolarity (increase).
ii) Urine:-sugar; ketones
iii) ECG
iv) Investigation to find source of infection:-
urine (RE/ME) + c/s; CBC; Blood c/s; CXR
D/D
• Metabolic acidosis
• Septicaemia
• Pancreatitis
• UTI
• Gastro-enteritis-> dehydration
AIM OF THERAPY
• i) Expansion of intravascular volume.
• ii) Correction of deficit in fluids.
• iii) Electrolyte & acid-base status.
• iv) Initiation of Insulin therapy to correct
hyperglycaemia
MANAGEMENT
• i) ABC of resucitation.
• ii) Fluid & electrolyte manage
fluids & electrolytes loss in DKA
components loss maint. req/day.
Water 100ml/kg usual maint.
Na 6mEq/kg 3mEq/kg
K 5mEq/kg 2mEq/kg
Cl 4mEq/kg 2mEq/kg
HCO3 3mEq/kg 0.7mEq/kg
%of dehydration is usually taken as 10%
• Calculation of deficit vol. & maintenance vol.
• Fluids should be given in such a way that it provides 50-
60% calculated deficit in 12 hours & rest 40-50% in next
24 hrs. This is v. imp in preventing central edema.
• Initial bolus is given as 20 ml/kg of isotonic (0.9% NS) in
1 hour.
• 2nd hour-20ml/kg of 0.45%NS + 20mEq/l of KCl
• After bolus- start 1/2NS and KCl 20-40mEq/l (3-12 hrs).
• After 12 hrs maintenance plus deficit vol. for next 24
hours. This is given as 1/5 NS & 40mEq/l of K
If blood glucose is 250-300mg/dl 5% glucose should be
added to prevent hypoglycemia.
• It is v.imp that till blood glucose is
>300mg/dl, no glucose containing fluid
should be given sips, orally should be
started.
• If serum K <3.5mEq/L add 40mEq/L to IV
fluid.
• 3.5-5 then add 30mEq/L
• 5-5.5 then add 20mEq/L
• &>5.5 then no KCl
Fluid therapy
Time amount/type of fluid
1 hour 20ml/kg of 0.9%NS
2 hour 20ml/kg of 0.45%NS+20mEq/L of
KCl
3-12 hour 1/2NS+30mEq/L of KCl(60% of
total fluid)
Next 24 hrs:-1/5NS+40mEq/L of KCl
+5%dextrose.(40% of total)
• Example
Wt=12kg; Dehydration 10%; Deficient=1200ml;
Maintenance=1100ml in 24 hours therefore 1650
ml in 36 hrs
Total 2850 ml
60% of this in 1st 12 hrs=1710ml
2nd bolus of 20 ml/kg=480ml
rest 1230ml
Rest 40%(1140)in next 24 hours.
Insulin therapy
• Continuous low dose insulin therapy.
• Bolus 0.1U/kg of regular insulin iv, after 1hr followed by
0.1 U/kg/hr by continuous infusion.
• When bolus glucose is 300mg/dl infusion can be
decrease to 0.05U/kg/hr
• Once acidosis is corrected continuous infusion can be
replaced by sc dose of 0.2-0.4U/kg every 6-8 hourly.
• RBS should be checked before giving each dose.
• If glucose con.increase then increase insulin dose by
50% & vice-versa.
Intermittent insulin therapy for DKA
• Blood glu. tot.insulin iv.dose sc freq.
• >600mg/dl 1U/kg 0.5U/kg 0.5 2-4hrly
• 300-600 0.5 0.25 0.25 2-4 ’’

• Others:
Bicarbonate therapy if pH <7.1 give bicarbonate
1mEq/L over 1 hour iv
SUPPORTIVE:-maintenance of hygiene
,posture,catheterization
• Antibiotics:- no role of prophylactic antibiotics. search
some of infection and manage accordingly.
• COMPLICATIONS:-
• I) central edema:- Rx-slow down infusion rate of fluid and
mannitol 1g/kg bolus over 4-6 hourly.
• II) Hypoglycaemia:-Rx 5-10% of glucose to iv fluids when
blood glucose 250-300mg/dl
• III) Hypokalemia:- prevent by adding KCl after 1st hr once
pts passes urine
• IV) Arrythemia due to decrease or increase of K and
decrease Ca
Monitoring
• Vital signs
• Blood glucose initially hourly till 300mg/dl
then 2 hrly.
• Urea & electrolyte- every 3-4 hr in 1st 12 hr
then 6 hrly
• Urinary glucose + ketone in each sample
• ECG
• Neurologic status
Steps in management
1)Conform diag:- Blood glucose, Na, K, pH
urine sugar,ketone & others
ICU care is needed if <2yrs unconscious, pH<7.0, blood
glucose>1000mg/dl
2)Start fluid – 20ml/kg of 0.9% NaCl over 1 hr
3)Reassess – find out ppt factors
4)Fluid therapy +insulin– start 0.1U/kg/h in 2nd hour
5)Measurement of blood glucose + electrolytes and Acid-
Base
6)Continue fluid + insulin therapy. If glucose is about
300mg/dl add glucose to fluid.
7)Once acidosis is corrected insulin can be
given sc
8)If acidosis is not corrected with fluids and
insulin 0.1U/kg/hr infusion—think of sepsis
9)After 4-6 hr of therapy especially in
younger children– suspect cerebral
edema.
10)Contimuous monitoring.

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