Diabetic Ketoacidosis

Dr.Salman Paris H. SpPD

RSUD Budhi Asih/FKUPVJ
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 (Kussmaul’s) 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-rays…etc , 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 cross-react 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, Ringer’s lactate or a plasma
expander as a bolus dose of 20-30 ml/kg. This can
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. Administer 0.9% Saline 10 ml/kg/hour for an
initial hour, to restore blood volume and renal
perfusion.
2. 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

don’t 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