Diabetic Ketoacidosis

Diabetic Ketoacidosis
Martin Osodo, M.O.I – Medical

Wards
Introduction
• Diabetic ketoacidosis (DKA) is a potentially
life- threatening complication in people with
diabetes mellitus.
• It happens predominantly in those with type 1
diabetes, but it can occur in those with type 2
diabetes under certain circumstances.
Definition
• DKA is defined as the presence of all three of
the following:
– Hyperglycemia (glucose >14 mg/dL)
– Ketosis,
– Acidemia (pH <7.3).

Classification of DKA
• DKA is generally categorized by the severity of the
acidosis.
– MILD – Venous pH < 7.3 and/or bicarbonate

concentration < 15 mmol/L
– MODERATE – Venous pH < 7.2 and/or

bicarbonate concentration < 10 mmol/L
– SEVERE – Venous pH < 7.1 and/or

bicarbonate concentration < 5 mmol/L
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 Kenya. Similar results were reported from
other African countries .
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
Pathophysiology
• Insulin is required for transport of glucose
into: Muscle, Adipose, Liver. It inhibits lipolysis
too.
• In absence of insulin
– Glucose accumulates in the blood.
– The body uses amino acids for gluconeogenesis
– It also converts fatty acids into ketone bodies :
Acetone, Acetoacetate, β-hydroxybutyrate
• Diabetic ketoacidosis arises because of a lack of insulin
in the body.
• The lack of insulin and corresponding elevation of
glucagon leads to increased release of glucose by the
liver(a process that is normally suppressed by insulin)
from glycogen via glycogenolysis and also through
gluconeogenesis.
• High glucose levels spill over into the urine, taking
water and solutes (such as sodium and potassium)
along with it in a process known as osmotic diuresis.
• This leads to polyuria, dehydration, and compensatory
thirst and polydipsia.
• The absence of insulin also leads to the release of
free fatty acids from adipose tissue (lipolysis),
which are converted through a process called
beta oxidation, again in the liver, into ketone
bodies (acetoacetate and β- hydroxybutyrate).
• β-Hydroxybutyrate can serve as an energy source
in the absence of insulin-mediated glucose
delivery, and is a protective mechanism in case of
starvation.
• The ketone bodies, however, have a low pKa and
therefore turn the blood acidic (metabolic
acidosis).
• The body initially buffers the change with the
bicarbonate buffering system, but this system is
quickly overwhelmed and other mechanisms
must work to compensate for the acidosis.
• One such mechanism is hyperventilation to lower
the blood carbon dioxide levels (a form of
compensatory respiratory alkalosis).
Clinical Presentation
• Symptoms
– Insidious increased thirst (ie, polydipsia) and urination
– Nausea and vomiting
– Generalized weakness and fatigability
– Altered consciousness is common
– Symptoms of associated intercurrent illnes
• Signs
– Signs of dehydration
– acetone odor
– Signs of acidosis
– Shallow rapid breathing or air hunger (Kussmaul or sighing respiration)
– Abdominal tenderness
– Disturbance of consciousness
– Signs of intercurrent illness
Lab. Investigations
• blood glucose
• UECs
• BGAs
• urinalysis for glucose, ketones, protein
• FHG, ESR
• ECG for hypo or hyperkalemia
• Others if indicated:Blood C/S, Urine for micro,
culture and sensitivity , CXR, Head CT/MRI.
Management
• Principles include
– Correct Dehydration and Electrolyte imbalance.
– Treat Hyperglycemia/Acidosis with IV Insulin
therapy
– Watch for complications
– Treat precipitants
Fluid Therapy
• Assume 10% dehydration ,Fluid replacement
should be gradual (24 hr)
• NS for first 4 hr.
– Administer 1 liter over the first 30 minutes.
– Administer 1 liter over the second hour.
– Administer 1 liter over the following 2 hours.
– Administer 1 liter every 4 hours, depending on the
degree of dehydration.
• Consider half NS thereafter.
• Change to D5 half NS when blood glucose ≤13
mmol/L
Insulin Therapy
• Subcutaneous absorption of insulin is reduced in DKA
because of dehydration; therefore, using IV or IM routes is
always preferable.
• Initial
– IV: 0.1 unit/kg/hr by continuous infusion after 1st hour of fliud
therapy
– Subsequent Double if no improvement in glucose or pH by 3 hr.
– Maximum glucose decline: 3 to 5 mmol/L/hr.
– At 15 mmol/L glucose, add dextrose to intravenous solutions (up
to 12.5%) as needed to maintain plasma glucose at 12- 15
mmol/L
• Continue insulin regimen until the academia is corrected
(pH >7.3 and/or HCO3 >18)
• Start subcutaneous insulin with a 1-hr overlap in the
intravenous.
Electrolytes Supplementation
• Potassium
– Monitor ECG
• Hypokalemia : Flattening T wave, widening of the QT interval, and
appearance of U waves
• Hyperkalemia : Tall, peaked symmetrical, T waves and shortening
of QT intervals
– If the K+ is <3.5 mEq/L, add 40 to 60 mEq/L; if 3.5 to 5, and
30 mEq/L; if >5.0, then hold K+ replacement
– After 3-5 hr. half of K+ replacement as K+ phosphate
• Sodium Bicarbonate
– Only use bicarbonate (HCO3-) for pH <7.0
– Add HCO3- slowly maximum 50 mEq/500 mL IV solution
(over 2-3 hr) Maximum HCO3- should be 50 mEq/500 mL
IV solution
Monitoring
• Flow sheet mantained tabulating mental status,
vital signs,insulin dose,fluid and electrolyte
administered and urine output
• Capillary glucose 1-2hrly,electrolytes especially

K+,bicarbonate and phosphate) and anion gap
every 4 hrly for first 24 hr
• Monitor BP, pulse respiration fluid intake and

output every 1-4 h
Complications of DKA
• Hypoglycemia
• Hypophosphasemic muscle weakness during recovery from DKA
• Acute tubular necrosis from severe dehydration
• Hemolysis due to acidosis
• Myoglobinuria due to acidosis
• Pulmonary edema and adult respiratory distress syndrome
secondary to fluid overload
• Cardiovascular complications ( seen more in adults than children)
• CNS complications:
– Thrombovascular phenomena (22 to dehydration and
hypercoagulability of DKA)
– cerebral edema.
Complications of DKA
•Shock
– If not improving with fluids •Cerebral Edema
r/o MI – First 24 hours
– Mental status changes
•Vascular thrombosis – May requireintubation
– Severe dehydration with hyperventilation
– Cerebral vessels
– Occurs hours to days after DKA
•Pulmonary Edema
– Result of aggressivefluid
resuscitation

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Diabetic Ketoacidosis

Martin Osodo, M.O.I – Medical

– Hyperglycemia (glucose >14 mg/dL)

– Acidemia (pH <7.3).

– MILD – Venous pH < 7.3 and/or bicarbonate

– MODERATE – Venous pH < 7.2 and/or

– SEVERE – Venous pH < 7.1 and/or

• Capillary glucose 1-2hrly,electrolytes especially

• Monitor BP, pulse respiration fluid intake and

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