1. Diabetic Ketoacidosis
Dr . S Ibrar Orakzai
Dr . S Ibrar Orakzai
Assistant Professor of Pediatric
Assistant Professor of Pediatric
Foundation University of Health Sciences
Foundation University of Health Sciences
2. 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%.
3. Epidemiology
DKA is reported in 2-5% of known type 1
DKA is reported in 2-5% of known type 1
diabetic patients in industrialized countries,
diabetic patients in industrialized countries,
while it occurs in 35-40% of such patients in
while it occurs in 35-40% of such patients in
Africa.
Africa.
DKA at the time of first diagnosis of diabetes
DKA at the time of first diagnosis of diabetes
mellitus is reported in only 2-3% in western
mellitus is reported in only 2-3% in western
Europe, but is seen in 95% of diabetic children
Europe, but is seen in 95% of diabetic children
in Sudan.
in Sudan.
4. Pathophysiology
Secondary to insulin deficiency, and the action of
counter-regulatory hormones, blood glucose
increases leading to hyperglycemia and glucosuria.
Glucosuria
Glucosuria causes an osmotic diuresis, leading to
causes an osmotic diuresis, leading to
water & Na loss.
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.
5. 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 and increased insensible water losses
due to tachypnea will worsen the state of
dehydration.
Electrolyte abnormalities are due to their loss in
urine & trans-membrane alterations following
acidosis & osmotic diuresis.
6. 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.
7. Pathophysiology/4
The dehydration can lead to decreased kidney
The dehydration can lead to decreased kidney
perfusion and acute renal failure.
perfusion and acute renal failure.
Accumulation of ketone bodies contributes to
Accumulation of ketone bodies contributes to
the abdominal pain and vomiting.
the abdominal pain and vomiting.
The increasing acidosis leads to acidotic
The increasing acidosis leads to acidotic
breathing and acetone smell in the breath and
breathing and acetone smell in the breath and
eventually causes impaired consciousness and
eventually causes impaired consciousness and
coma.
coma.
8. 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:
Omission of Insulin: 20%. This is due to:
Non-availability (poor countries)
fear of hypoglycemia
fear of hypoglycemia
fear of weight gain
fear of weight gain
stress of chronic disease
stress of chronic disease
9. DIAGNOSIS
You should suspect DKA if a diabetic
You should suspect DKA if a diabetic
patient presents with:
patient presents with:
Dehydration.
Dehydration.
Acidotic (Kussmaul’s) breathing, with a fruity
Acidotic (Kussmaul’s) breathing, with a fruity
smell (acetone).
smell (acetone).
Abdominal pain &or distension.
Abdominal pain &or distension.
Vomiting.
Vomiting.
An altered mental status ranging from
An altered mental status ranging from
disorientation to coma.
disorientation to coma.
10. 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.
11. 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.
.
12. 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.
13. Quick Diagnosis
Known diabetic children confirm hyperglycemia,
Known diabetic children confirm hyperglycemia,
ketonuria & acidosis.
ketonuria & acidosis.
Newly diagnosed diabetic children be careful not to miss
Newly diagnosed diabetic children be careful not to miss
because it may mimic serious infections like meningitis.
because it may mimic serious infections like meningitis.
Both
Both Hyperglycemia (using glucometer) glycosuria, &
Hyperglycemia (using glucometer) glycosuria, &
ketonuria (with strips) must be done in the ER and
ketonuria (with strips) must be done in the ER and
treatment started, without waiting for Lab results which
treatment started, without waiting for Lab results which
may be delayed.
may be delayed.
14. Baseline Investigations
The initial Lab evaluation includes:
The initial Lab evaluation includes:
Plasma & urine levels of glucose & ketones.
Plasma & urine levels of glucose & ketones.
ABG, U&E (including Na, K, Ca, Mg, Cl, PO4,
ABG, U&E (including Na, K, Ca, Mg, Cl, PO4,
HCO3), & arterial pH (with calculated anion gap
HCO3), & arterial pH (with calculated anion gap
Complete Blood Count with differential.
Complete Blood Count with differential.
Further tests e.g., cultures, X-rays…etc , are done
Further tests e.g., cultures, X-rays…etc , are done
when needed.
when needed.
15. Pitfalls in DKA
High WCC: may be seen in the absence of
: may be seen in the absence of
infections.
infections.
BUN: may be elevated with prerenal azotemia
may be elevated with prerenal azotemia
secondary to dehydration.
secondary to dehydration.
Creatinine: some assays may cross-react with
some assays may cross-react with
ketone bodies, so it may not reflect true renal
ketone bodies, so it may not reflect true renal
function.
function.
Serum Amylase: is often raised, & when there is
Serum Amylase: is often raised, & when there is
abdominal pain, a diagnosis of pancreatitis may
abdominal pain, a diagnosis of pancreatitis may
mistakenly be made.
mistakenly be made.
16. 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.
17. Fluids replacement
Determine hydration status
Determine hydration status:
:
A.
A. Hypovolemic shock:
Hypovolemic shock:
administer 0.9% saline, Ringer’s lactate or a plasma
administer 0.9% saline, Ringer’s lactate or a plasma
expander as a bolus dose of 20-30 ml/kg. This can
expander as a bolus dose of 20-30 ml/kg. This can
be repeated if the state of shock persists.
be repeated if the state of shock persists. Once the
Once the
patient is out of shock, you go to the 2
patient is out of shock, you go to the 2nd
nd
step of
step of
management.
management.
18. Fluids replacement/2
B- Dehydration without shock:
B- Dehydration without shock:
1.
1. Administer 0.9% Saline 10 ml/kg/hour for an
Administer 0.9% Saline 10 ml/kg/hour for an
initial hour, to restore blood volume and renal
initial hour, to restore blood volume and renal
perfusion.
perfusion.
2.
2. The remaining deficit should be added to the
The remaining deficit should be added to the
maintenance, & the total being replaced over 36-
maintenance, & the total being replaced over 36-
48 hours.
48 hours.
19. 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.
Total fluid is calculated as
85ml/kg plus maintenance fluid/24 hours
20. 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.
21. Insulin Therapy/2
Continue the Insulin infusion until acidosis is
Continue the Insulin infusion until acidosis is
cleared:
cleared:
pH > 7.3.
pH > 7.3.
Bicarbonate > 15 mmol/l
Bicarbonate > 15 mmol/l
Normal anion gap 10-12.
Normal anion gap 10-12.
22. Correction of Acidosis
Insulin therapy stops lipolysis and
Insulin therapy stops lipolysis and
promotes the metabolism of ketone bodies.
promotes the metabolism of ketone bodies.
This together with correction of dehydration
This together with correction of dehydration
normalize the blood PH.
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.
As acidosis is corrected, urine KB appear to rise.
Urine KB are not of prognostic value in DKA.
Urine KB are not of prognostic value in DKA.
23. Correction of Electrolyte Imbalance
Regardless of K conc. at presentation, total body K
Regardless of K conc. at presentation, total body K
is low. So, as soon as the urine output is restored,
is low. So, as soon as the urine output is restored,
potassium supplementation must be added to IV
potassium supplementation must be added to IV
fluid at a conc.
fluid at a conc. of 20-40 mmol/l
24. Potassium
If K conc. < 2.5, administer 1mmol/kg of
If K conc. < 2.5, administer 1mmol/kg of
KCl in IV saline over 1 hour. Withhold
KCl in IV saline over 1 hour. Withhold
Insulin until K conc. becomes> 2.5 and
Insulin until K conc. becomes> 2.5 and
monitor K conc. hourly.
monitor K conc. hourly.
If serum potassium is 6 or more, do not give
If serum potassium is 6 or more, do not give
potassium till you check renal function and
potassium till you check renal function and
patients passes adequate urine.
patients passes adequate urine.
25. 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.
27. Cerebral Edema
Clinically apparent Cerebral edema occurs in 1-2%
Clinically apparent Cerebral edema occurs in 1-2%
of children with DKA. It is a serious complication
of children with DKA. It is a serious complication
with a mortality of > 70%. Only 15% recover
with a mortality of > 70%. Only 15% recover
without permanent damage.
without permanent damage.
Typically it takes place 6-10 hours after initiation of
Typically it takes place 6-10 hours after initiation of
treatment, often following a period of clinical
treatment, often following a period of clinical
improvement.
improvement.
28. 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.
29. 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.
30. Treatment of C. Edema
Reduce IV fluids
Reduce IV fluids
Raise foot of Bed
Raise foot of Bed
IV Mannitol
IV Mannitol
Elective Ventilation
Elective Ventilation
Dialysis if associated with fluid overload or renal
Dialysis if associated with fluid overload or renal
failure.
failure.
Use of IV dexamethasone is not recommended.
Use of IV dexamethasone is not recommended.
![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.](https://image.slidesharecdn.com/436511-250310032136-a0db2619/85/43651-1-ppt-diabetic-keto-acidosis-in-ediatrics-10-320.jpg)
