1. Diabetic Ketoacidosis
ICD-10 CODE E10.1
DEFINITION
Diabetic ketoacidosis (DKA) is a life-threatening complication of diabetes mellitus resulting from
severe insulin deficiency and manifested by severe dehydration, hyperglycemia, ketonemia,
ketonuria, and metabolic acidosis.
PHYSICAL FINDINGS & CLINICAL PRESENTATION
• Evidence of dehydration (tachycardia, hypotension, dry mucous membranes, sunken eyeballs,
poor skin turgor)
• Clouding of mental status
• Tachypnea with air hunger (Kussmaul’s respiration)
• Fruity breath odour (caused by acetone)
• Lipemia retinalis in some patients
• Possible evidence of precipitating factors (infected wound, pneumonia)
• Abdominal tenderness in some patients.
ETIOLOGY
• Metabolic decompensation in diabetics usually precipitated by an infectious process (up to 40%
of cases).
• Poor compliance with insulin therapy and severe medical illness (e.g., CVA, MI) are other
common causes.
• Cocaine abuse has been reported as a risk factor for DKA in adult and teenage patients,
particularly in patients with multiple admissions.
DIFFERENTIAL DIAGNOSIS
• Hyperosmolar Nonketotic state
• Alcoholic ketoacidosis
• Uremic acidosis
• Metabolic acidosis caused by methyl alcohol or ethylene glycol
• Salicylate poisoning
WORKUP
• Laboratory evaluation to confirm diagnosis and evaluate precipitating factors
• ECG to evaluate electrolyte abnormalities and rule out myocardial ischemia or infarction as a
contributing factor
LABORATORY TESTS
• Glucose level reveals severe hyperglycemia (serum glucose generally >14 mmol/l); urine/serum
ketones positive.
• Arterial blood gases reveal acidosis: arterial pH usually <7.30 with PCO2 <40 mm Hg.
• Serum electrolytes:

2. 1. Serum bicarbonate is usually <18 mmol/l.
2. Serum potassium may be low, normal, or high. There is always significant total body
potassium depletion regardless of the initial potassium level.
3. Serum sodium is usually decreased as a result of hyperglycemia, dehydration, and
lipemia.
• Complete blood count with differential, urinalysis, and urine and blood cultures to rule out
infectious precipitating factor.
• Serum calcium, magnesium, and phosphorus; the plasma phosphate and magnesium levels may
be significantly depressed and should be rechecked within 24 hr because they may decrease
further with correction of DKA.
• Blood urea nitrogen and creatinine generally reveal significant dehydration.
• Amylase and liver enzymes should be checked in patients with abdominal pain.
IMAGING STUDIES
Chest radiographs are helpful to rule out infectious process.
NONPHARMACOLOGIC THERAPY
• Monitor mental status, vital signs, and urine output hourly until improved, then monitor q2-4h.
• Monitor electrolytes, ph, renal function, and ketonuria and glucose level.
ACUTE GENERAL Rx
Fluid replacement (usual deficit is 6 to 8 L):
1. Do not delay fluid replacement until laboratory results have been received. Fluid deficits are
typically 100 ml/kg of body weight.
2. The initial fluid replacement should be with 0.9% NS until blood pressure and organ perfusion
are restored (usually ≥1 L). In patients with severe hypernatremia (serum sodium >160 mEq/L),
0.45% saline infusion can be used. Careful monitoring for fluid overload is necessary in elderly
patients and those with a history of congestive heart failure.
3. The rate of fluid replacement varies with the age of the patient and the presence of significant
cardiac or renal disease.
• The usual rate of infusion is 1 L over the first hour and 300-500 ml/hr for the next 12 hr.
• Continue the infusion using NS until the serum glucose level is <14mmol/l, then change
the hydrating solution to D5W to prevent hypoglycemia, replenish free water, and
introduce additional glucose substrate (necessary to suppress lipolysis and ketogenesis).
Insulin administration:
1. Insulin replacement should not be started until serum potassium is >3.3 mEq/L to
prevent life-threatening hypokalemia. (Check ABG Potassium level)

3. The patient should be given an initial loading IV bolus of 0.15 to 0.2 U/kg of regular insulin
followed by a constant infusion at a rate of 0.1 U/kg/hr (e.g., 50 U of regular insulin in 200 ml of
0.9% saline solution at 20 ml/hr equals 5 U/hr for a 50-kg patient).
2. Monitor serum glucose hourly for the first 2 hr, and then monitor q2-4h.
3. The goal is to decrease serum glucose level by 5 mmol/l/hr (after an initial drop because of
rehydration); if the serum glucose level is not decreasing at the expected rate, increase infusion
rate by 1 units/hr (4ml/hr).
4. When the serum glucose level approaches 14mmol/l, decrease the rate of insulin infusion by
halve and continue this rate until the patient has received adequate fluid replacement, ph and
HCO-
3 are normal, and ketones have cleared.
5. Approximately 120 min before stopping the IV insulin infusion, administer a SC dose of regular
insulin.
Electrolyte replacement:
• Potassium replacement:
1. As a rule of thumb, potassium replacement may be started when there is no ECG
evidence of hyperkalemia.
2. In patients with normal renal function, potassium replacement can be started by adding
20 mmol KCl/L of IV hydrating solution if serum potassium is 3, 5 to 5, 5 mEq/L. In
patients with severe hypokalemia (potassium <3,5mmol/L), give 40 mEq of potassium/hr
until potassium is >3,5mmol/L.
3. Monitor serum potassium level hourly for the first 2 hr, and then monitor q2-4h.
• Phosphate replacement is indicated only in the presence of significant hypophosphatemia.
• Magnesium replacement is indicated only in the presence of significant hypomagnesemia or
refractory hypokalemia.
Bicarbonate therapy:
• Give 50 mmol/l NaHCO3 in 200 ml 0.9% saline over 1 h
Until pH increases to >7.
Patients with DKA should be admitted to a high care unit. Intensive care admition must be
considered in patients with altered level of consciousness, severe metabolic acidosis not
responding well to treatment and in those requiring support of vital organs.
COMMENTS
• Although DKA occurs more commonly in type 1 diabetes mellitus, a significant proportion
(>20%) occurs in patients with type 2 diabetes.
• 20% of DKA admissions involve newly diagnosed diabetics.

4. • Potential complications of DKA therapy include hypoglycemia, cerebral edema, and cardiac
arrhythmias.

5. Recommended fluids
0.9% Sodium chloride 1L Over 1 hour. Next
0.9% Sodium chloride 1L Over 2 hours. Next
0.9% Sodium chloride 1L Over 3 hour. Next
0.9% Sodium chloride 1L Over 4 hours. Next
0.9% Sodium chloride 1L Every 6
hours
Bicarbonate therapy
FLUIDS AND ELECTROLYTES
Hypotensive patient (<90mmHg)
- Severely depleted – give 500ml of
0.9% sodium chloride IV over 15 to 20
minutes
- Repeat until SBP >90mmHg (Maximum
of 3 doses)
- Do not give potassium chloride in first
litre or if serum potassium (K+) > 5.5
mmol/L
- All subsequent fluid for the next 24
hours should contain KCl unless urine
output is <30ml/hr or serum potassium
remains in excess of 5.5mmol/l
Not Hypotensive (= >90mmHg)
Recommended
potassium replacement
Potassium Level Replacement Litre Fluid
> 5,5 mmol/l nil
3,5 – 5,5 mmol/l 20 mmol/l
< 3,5 mmol /l 40 mmol/l
When BG less than 14mmol/L
Start: 5% de Glucose 1l over 6 hours.
Start: 10% glucose 1 l over 6 hours.
-Insulin replacement should not be-Insulin replacement should not be
started until serum potassium is >3.3
mmol/L to prevent life-threateningmmol/L to prevent life-threateningmmol/L to prevent life-threatening
hypokalemia. (Check ABG Potassium
- Initial IV bolus of 0.2 U/kg of regular
50
units Actrapid or Humulin Rid or Humulin R,, made uup
to 200 ml with 0.9% Sodium chloride.e.
kg/h.
@20mls /hr =5u/hr for a 50kgs patient
- sulin
- ol/h.
its/h
-When BG level approaches 14mmol/l,
decrease the rate of insulin infusion bydecrease the rate of insulin infusion by
halve
When Stable (pH>7.3)
- Patient is eating and drinking,
Change to S/C insulin regimen.
- Stop IV insulin pump after 2 hours
after the first sc insulin dose
Monitoring
Level of consciousness, Pulse, BP, O2
sats, urine output and capillary
glucose should be monitored and
recorded in the notes
- Measure glucose hourly
- Blood gases (0, 2, 4, 8 and 12
hrs.)
And before stopping fixed rate
insulin regime.
- Monitor hourly urine output
- Check magnesium level
Remember
CXR and ECG
- Look for infections.
- Treat precipitant factors.
- Use of prophylactic anticoagulation in
comatose, obese and hyperosmolar
patients
- Please use the patient data
flowsheet
MANAGEMENT OF DIABETIC KETOACIDOSIS.DEPARTMENT
OF INTERNAL MEDICINE.KIMBERLEY HOSPITAL
COMPLEX.2011

6. DKA Patient data flow sheet
Patient name: _________________________ Folder No: _______________
Date: __________
Hour
Vital signs
Chemistries
Blood Gases
Insulin (units in past hour)
Fluid/Metabolites (Past hours)
Output
Other
Level of consciousness
Temperature
Pulse
Respiratory rate
Blood pressure
Capillary Glucose
Urine Ketones
Serum Na+
Serum K +
Serum Cl -
Serum HCO3
Urea
pH Specify venous (V) or Arterial (A)
pO2
O2 sat
pCO2
Route
IV
SC
IM
0.45 percent NaCl (ml)
0.9 percent NaCl (ml)
5 percent dextrose (ml)
Others
Urine (ml)

7. DKA Patient data flow sheet
Patient name: _________________________ Folder No: _______________
Date: __________
Hour
Vital signs
Chemistries
Blood Gases
Insulin (units in past hour)
Fluid/Metabolites (Past hours)
Output
Other
Level of consciousness
Temperature
Pulse
Respiratory rate
Blood pressure
Capillary Glucose
Urine Ketones
Serum Na+
Serum K +
Serum Cl -
Serum HCO3
Urea
pH Specify venous (V) or Arterial (A)
pO2
O2 sat
pCO2
Route
IV
SC
IM
0.45 percent NaCl (ml)
0.9 percent NaCl (ml)
5 percent dextrose (ml)
Others
Urine (ml)