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ketoacidosis
Dr. Mabruka Belaid
contents
Case presentation.
DKA Pathophysiology.
Objectives
1. To describe the features of a typical case of DKA.
Case Scenario
A 6 y/o female (~24 kg)
presents to the ED with a one-day history of emesis
and lethargy.
Vitals show T 37C, HR 110, RR 30 BP 95/60.
Patient is lethargic, but oriented x 3.
Exam reveals the odor of acetone on the breath, dry
lips, but otherwise unremarkable
Labs: BG 470 pH 7.05 PaCO2 22, PaO2 100, BE -20
, Na+ 130, K + 5.4, HCO3 7. Urine shows 4+ ketones
Case Scenario
What is your assessment?
What is your diagnosis ?
How much fluid would you administer as a
bolus?
Would you administer bicarbonate?
How much insulin would you administer?
What IVF would you start? At what rate?
Case Scenario
Clinical assessment :
dehydration .
Investigations:
1. Hyperglycemia
2. Hyponatremia
3. Metabolic acidosis
4. ketonaemia &Ketonuria
Diagnosis :
DKA
Pathophysiology
Insulin Deficiency is the Primary defect
Stress hormones accelerate and exaggerate the
rate and magnitude of metabolic
decompensation
It is the resulting accelerated catabolic state that
gives rise to the classical picture of DKA with:
hyperglycaemia, hyperketonaemia, &
hyperosmolality.
Pathophysiology
Hyperglycaemia is due to impaired peripheral
uptake of glucose with increased hepatic
gluconeogenesis and glycogenolysis, whereas
ketonaemia occurs secondary to increased
lipolysis.
both contribute to the ensuing hyperosmolar
state. The resultant osmotic diuresis leads to
dehydration and loss of total body electrolytes.
Pathophysiology
Biochemical criteria
Hyperglycemia (BG => 200 mg\dl)
Venous PH < 7.3 or
bicarbonate < 15 mmol\L
Ketonemia and ketonuria
Clinical manifestations
of DKA
Polyuria , polydipsia , Nausea
,vomiting, and dehydration
abdominal pain mimicking an
acute abdomen.
More severe cases include Kussmaul
respirations, odor of acetone on the
breath
Progressive impaired consciousness.
Fever only when infection is present
1- General Resuscitation :
A, B, C.
2- History, examination .
Conscious Level.
Degree of Dehydration:
mild, 3%
Full Examination .
MANAGEMENT :
ELEMENTS OF THERAPY:
Fluids treat shock, then sufficient to reverse
dehydration and replace ongoing losses (will
correct hyperglycemia).
Insulin sufficient to suppress ketosis, reverse
acidosis, promote glucose uptake and utilization
(will stop ketosis).
Electrolytes replace profound Na+ and K+
losses .
1. FLUIDS :
a) Volume of fluid By this stage, the circulating volume should have
been restored and the child no longer in shock.
If not, give a further 10 ml/kg 0.9% saline (to a
maximum of 30 ml/kg) over 30 minutes.
Fluid Requirement =
Maintenance + Deficit fluid already given
2. POTASSIUM :
K levels in the blood will fall once
insulin is commenced.
Potassium replacement should be given
as 50 % Kcl & 50% Potassium
phosphate at concentration 20 -40
meq/l
Check U & E's 2 hours after
resuscitation is begun and then at least
4 hourly, and alter potassium
replacements accordingly.
3. INSULIN :
There is some evidence that cerebral oedema is
more likely if insulin is started early.
Therefore DO NOT start insulin until IVF have
been running for at least an hour.
Continuous low-dose IV infusion is the preferred
method ,run at 0.05 - 0.1 units/kg/hour .
4. BICARBONATE :
This is rarely, if ever, necessary.
Treatment monitoring
Blood glucose should be measured hourly .
Electrolytes , venous pH should be
repeated 2 -3 hours.
Case Scenario
A 6 y/o female (~24 kg)
presents to the ED with a one-day history of emesis
and lethargy.
Vitals show T 37C, HR 110, RR 30 BP 95/60.
Patient is lethargic, but oriented x 3.
Exam reveals the odor of acetone on the breath, dry
lips, but otherwise unremarkable
Labs: BG 470 pH 7.05 PaCO2 22, PaO2 100, BE -20
, Na+ 130, K + 5.4, HCO3 7. Urine shows 4+ ketones
Case Scenario
What is your assessment?
What is your diagnosis ?
How much fluid would you administer as a
bolus?
Would you administer bicarbonate?
How much insulin would you administer?
What IVF would you start? At what rate?
Complications of DKA
1) Cerebral Edema
Risk factors:
Age <5 years
High BUN (severe dehydration)
Severity of acidosis
Bicarbonate administration
New-diagnosis diabetes
Na levels dont rise as expected with
treatment
CEREBRAL OEDEMA :
The signs and symptoms
headache & slowing of heart rate
CEREBRAL OEDEMA :
MANAGEMENT :
The following measures should be taken immediately
while arranging transfer to PICU
exclude hypoglycaemia as a possible cause of any
behaviour change .
give hypertonic (2.7%) saline (5mls/kg over 5-10
mins) or Mannitol 0.5 1.0 g/kg stat . This needs to
be given as soon as possible if warning signs occur (eg
headache or pulse slowing).
restrict IV fluids to 1/2 maintenance and replace
deficit over 72 rather than 48 hours .
Complications of DKA
2 )Thrombosis .
Dehydration, low flow state.
Avoid central lines if possible.
3 ) Acute tubular necrosis with acute renal failure
sever dehydration .
4)Arrythemias caused by electrolyte abnormalities.
5 ) pulmonary edema & bowel ischemia.
6 )periphral edema occurs commonly 24 to 48
hours after therapy is initiated
( related to ADH & Aldosterone )
Points to remember
DKA is caused by either relative or absolute
insulin deficiency.
Begin with fluid replacement before starting
insulin therapy.