Diabetic Ketoacidosis: Indra Gunawan Limadhy Rspad Gatot Soebroto

Diabetic
Ketoacidosis
Indra Gunawan Limadhy
RSPAD GATOT SOEBROTO
Introduction
DKA is a serious acute complications of

Diabetes Mellitus. It carries significant
risk of death and/or morbidity especially
with delayed treatment.
The prognosis of DKA is worse in the
extremes of age, with a mortality rates
of 5-10%.
With the new advances of therapy, DKA
mortality decreases to > 2%. Before
discovery and use of Insulin (1922) the
mortality was 100%.
Epidemiology
DKA is reported in 2-5% of known type

1 diabetic patients in industrialized
countries, while it occurs in 35-40%
of such patients in Africa.
DKA at the time of first diagnosis of
diabetes mellitus is reported in only
2-3% in western Europe, but is seen
in 95% of diabetic children in Sudan.
Similar results were reported from
other African countries .
Consequences
The latter observation is annoying
because it implies the following:
The late diagnosis of type 1 diabetes
in many developing countries
particularly in Africa.
The late presentation of DKA, which
is associated with risk of morbidity
& mortality
Death of young children with DKA
undiagnosed or wrongly diagnosed as
malaria or meningitis.
Pathophysiology
Secondary to insulin deficiency, and the

action of counter-regulatory hormones,
blood glucose increases leading to
hyperglycemia and glucosuria. Glucosuria
causes an osmotic diuresis, leading to
water & Na loss.
In the absence of insulin activity

the body fails to utilize glucose
as fuel and uses fats instead. This
leads to ketosis.
Pathophysiology/2
The excess of ketone bodies will cause

metabolic acidosis, the later is also
aggravated by Lactic acidosis caused by
dehydration & poor tissue perfusion.
Vomiting due to an ileus, plus increased
insensible water losses due to tachypnea
will worsen the state of dehydration.
Electrolyte abnormalities are 2ry to
their loss in urine & trans-membrane
alterations following acidosis & osmotic
diuresis.
Pathophysiology/3
Because of acidosis, K ions enter the

circulation leading to hyperkalemia, this
is aggravated by dehydration and renal
failure.
So, depending on the duration of DKA,
serum K at diagnosis may be high, normal or
low, but the intracellular K stores are
always depleted.
Phosphate depletion will also take place
due to metabolic acidosis.
Na loss occurs secondary to the
hyperosmotic state & the osmotic diuresis.
Pathophysiology/4
The dehydration can lead to decreased

kidney perfusion and acute renal
failure.
Accumulation of ketone bodies
contributes to the abdominal pain and
vomiting.
The increasing acidosis leads to
acidotic breathing and acetone smell
in the breath and eventually causes
impaired consciousness and coma.
Precipitating Factors
New onset of type 1 DM: 25%
Infections (the most common cause): 40%
Drugs: e.g. Steroids, Thiazides,
Dobutamine &
Turbutaline.
Omission of Insulin: 20%. This is due to:
Non-availability (poor countries)

fear of hypoglycemia
rebellion of authority
fear of weight gain
stress of chronic disease
DIAGNOSIS
You should suspect DKA if a

diabetic patient presents with:
Dehydration.
Acidotic (Kussmauls) breathing,
with a fruity smell (acetone).
Abdominal pain &\or distension.
Vomiting.
An altered mental status ranging
from disorientation to coma.
DIAGNOSIS/2
To diagnose DKA, the following criteria must
be
fulfilled :
1. Hyperglycemia: of > 300 mg/dl & glucosuria
2. Ketonemia and ketonuria
3. Metabolic acidosis: pH < 7.25,
serum
bicarbonate < 15 mmol/l. Anion gap >10.
Anion gap= [Na]+[K] [Cl]+[HCO3].
This is usually accompanied with severe
dehydration and electrolyte imbalance.
Management
The management steps of DKA includes:
Assessment of causes & sequele of DKA by taking

a short history & performing a scan
examination.
Quick diagnosis of DKA at the ER.
Baseline investigations.
Treatment, Monitoring & avoiding complications.
Transition to outpatient management.
Assessment
History:
Symptoms of hyperglycemia, precipitating
factors ,
diet and insulin dose.
Examination:
Look for signs of dehydration, acidosis, and
electrolytes imbalance, including shock,
hypotension, acidotic breathing, CNS status
etc.
Look for signs of hidden infections (Fever
strongly suggests infection) and If
possible, obtain
accurate weight before starting treatment.
Quick Diagnosis
Known diabetic children confirm D
hyperglycemia, K ketonuria & A acidosis.
Newly diagnosed diabetic children be
careful not to miss because it may mimic
serious infections like meningitis.
Both Hyperglycemia (using glucometer)

glycosuria, & ketonuria (with strips) must be
done in the ER and treatment started, without
waiting for Lab results which may be delayed.
Baseline
Investigations
The initial Lab evaluation includes:

Plasma & urine levels of glucose &
ketones.
ABG, U&E (including Na, K, Ca, Mg, Cl,
PO4, HCO3), & arterial pH (with calculated
anion gap).
Venous pH is as accurate as arterial (an
error of 0.025 less than arterial pH)
Complete Blood Count with differential.
Further tests e.g., cultures, X-raysetc ,
are done when needed.
Pitfalls in DKA
High WCC: may be seen in the

absence of infections.
BUN: may be elevated with prerenal
azotemia secondary to dehydration.
Creatinine: some assays may crossreact with ketone bodies, so it may
not reflect true renal function.
Serum Amylase: is often raised, &
when there is abdominal pain, a
diagnosis of pancreatitis may
mistakenly be made.
Treatment
Principles of Treatment:
Careful replacement of fluid deficits.

Correction of acidosis & hyperglycemia
via Insulin administration.
Correction of electrolytes imbalance.
Treatment of underlying cause.
Monitoring for complications of
treatment.
Manage DKA in the PICU. If not available
it can be managed in the special care
room of the pediatric inpatient ward.
Fluids replacement
Determine hydration status:
A.
Hypovolemic shock:
administer 0.9% saline, Ringers lactate

plasma
expander as a bolus dose of 20-30 ml/kg.
can
or a
This
be repeated if the state of shock persists.

Once the
patient is out of shock, you go to the 2nd step
of
management.
Fluids replacement/2
B- Dehydration without shock:
1.
2.
Administer 0.9% Saline 10 ml/kg/hour

for an initial hour, to restore
blood volume and renal perfusion.
The remaining deficit should be
added to the maintenance, & the
total being replaced over 36-48
hours. To avoid rapid shifts in
serum osmolality 0.9% Saline can be
used for the initial 4-6 hours,
followed by 0.45% saline.
Fluids replacement/3
When serum glucose reaches

250mg/dl
change fluid to 5%
dextrose with 0.45 saline, at a
rate that allow complete
restoration in 48 hours, & to
maintain glucose at 150-250mg/dl.
Pediatric saline 0.18% Na Cl
should not be used even in young
children.
Insulin Therapy
start infusing regular insulin at a rate of
0.1U/kg/hour using a syringe pump. Optimally,
serum glucose should decrease in a rate no
faster
than 100mg/dl/hour.
If serum glucose falls < 200 prior to
correction
of acidosis, change IV fluid from D5 to D10,
but
dont decrease the rate of insulin infusion.
The use of initial bolus of insulin (IV/IM)
is controversial.
Insulin Therapy/2
Continue the Insulin infusion
until acidosis is
cleared:
pH > 7.3.
Bicarbonate > 15 mmol/l
Normal anion gap 10-12.
Correction of
Acidosis
Insulin therapy stops lipolysis and
promotes the metabolism of ketone bodies.

This together with correction of
dehydration normalize the blood PH.
Bicarbonate therapy should not be used
unless severe acidosis (pH<7.0) results in
hemodynamic instability. If it must be
given, it must infused slowly over several
hours.
As acidosis is corrected, urine KB appear
to rise. Urine KB are not of prognostic
value in DKA.
Insulin Therapy/3
If no adequate settings (i.e. no
infusion or syringe pumps & no ICU
care which is the usual situation
in many developing countries) Give
regular Insulin 0.1 U/kg/hour IM
till acidosis disappears and blood
glucose drops to <250 mg/dl, then
us SC insulin in a dose of 0.25
U/kg every 4 hours.
When patient is out of DKA return
to the previous insulin dose.
Correction of Electrolyte
Imbalance
Regardless of K conc. at presentation,

total body K is low. So, as soon as the
urine output is restored, potassium
supplementation must be added to IV fluid
at a conc. of 20-40 mmol/l, where 50% of
it given as KCl, & the rest as potassium
phosphate, this will provide phosphate
for replacement, & avoids excess
phosphate (may precipitate hypocalcaemia)
& excess Cl (may precipitate cerebral
edema or adds to acidosis).
Potassium
If K conc. < 2.5, administer 1mmol/kg
of
KCl in IV saline over 1 hour. Withhold
Insulin until K conc. becomes> 2.5 and
monitor K conc. hourly.
If serum potassium is 6 or more, do
not give potassium till you check
renal function and patients passes
adequate urine.
Monitoring
A flow chart must be used to monitor
fluid
balance & Lab measures.
serum glucose must be measured hourly.

electrolytes also 2-3 hourly.
Ca, Mg, & phosphate must be measured
initially & at least once during therapy.
Neurological & mental state must
examined frequently, & any complaints of
headache or deterioration of mental status
should prompt rapid evaluation for
possible cerebral edema.
Complications
Cerebral Edema
Intracranial thrombosis or
infarction.
Acute tubular necrosis.
peripheral edema.
Cerebral Edema
Clinically apparent Cerebral edema

occurs in 1-2% of children with DKA.
It is a serious complication with a
mortality of > 70%. Only 15% recover
without permanent damage.
Typically it takes place 6-10 hours
after initiation of treatment, often
following a period of clinical
improvement.
Causes of Cerebral
Edema
The mechanism of CE is not fully understood,
but many factors have been implicated:

rapid and/or sharp decline in serum
osmolality with treatment.
high initial corrected serum Na
concentration.
high initial serum glucose concentration.
longer duration of symptoms prior to
initiation of treatment.
younger age.
failure of serum Na to raise as serum
glucose falls during treatment.
Presentations of C.
Edema
Cerebral Edema Presentations
include:
deterioration of level of
consciousness.
lethargy & decrease in arousal.
headache & pupillary changes.
seizures & incontinence.
bradycardia. & respiratory arrest when
brain stem herniation takes place.
Treatment of C. Edema
Reduce IV fluids
Raise foot of Bed
IV Mannitol
Elective Ventilation
Dialysis if associated with
fluid overload or renal failure.
Use of IV dexamethasone is not
recommended.
The End

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Diabetic

DKA is a serious acute complications of

DKA is reported in 2-5% of known type

Secondary to insulin deficiency, and the

In the absence of insulin activity

The excess of ketone bodies will cause

Because of acidosis, K ions enter the

The dehydration can lead to decreased

Non-availability (poor countries)

You should suspect DKA if a

Assessment of causes & sequele of DKA by taking

Quick diagnosis of DKA at the ER.

Treatment, Monitoring & avoiding complications.

Transition to outpatient management.

Both Hyperglycemia (using glucometer)

The initial Lab evaluation includes:

High WCC: may be seen in the

Careful replacement of fluid deficits.

Determine hydration status:

administer 0.9% saline, Ringers lactate

be repeated if the state of shock persists.

Administer 0.9% Saline 10 ml/kg/hour

When serum glucose reaches

Bicarbonate > 15 mmol/l

Normal anion gap 10-12.

promotes the metabolism of ketone bodies.

Regardless of K conc. at presentation,

serum glucose must be measured hourly.

Clinically apparent Cerebral edema

but many factors have been implicated:

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