Diabetic Ketoacidosis

and Hyperglycemia
Valerie Robinson, D.O.

Hyperglycemia

Type 1 DM, Type 2 DM, Gestational Diabetes

May present with polyuria, polydipsia, weight loss
May present with DKA
Type 1: usually in children with rapid onset. Caused by
autoimmune pancreatic -cell destruction, or idiopathic
Type 2: usually in adults with insidious onset. Caused
by insulin resistance, insulin secretory defect
Genetic and environmental factors influence
development of hyperglycemia.
The main goals of treatment are to alleviate symptoms,
minimize the development of long-term complications,
enhance the patient's quality of life, and reduce the risk
of death.

Complications of
Hyperglycemia
May lead to DKA, and Hyperosmolar
Hyperglycemic State.
Macrovascular disease CAD, MI, CVA, PAD
Diabetic foot ulcers
Microvascular disease nephropathy,
retinopathy, neuropathy, Charcots foot, ED
Increased risk of infxns and decreased healing
Gestational preeclampsia, SAB, premature
labor, polyhydramnios, macrosomia, RDS

What is DKA?
Severe electrolyte imbalance with
dehydration
Severe insulin shortage
Usually occurs in type 1 but may also occur in
type 2
May be the initial presentation of diabetes
mellitus
May be brought on by an infection or another
precipitating factor
trauma, CVD, pancreatitis, drugs, ETOH, poor diet

Signs and Symptoms

Fruity odor to breath (exhaled acetone)

Shock
Abdominal pain (ileus or delayed emptying)
Altered consciousness
Nausea/Vomiting
Dehydration
Polyuria
Polydipsia
Kussmaul breathing (compensatory
hyperventilation)

Pathogenesis
Pancreatic islet cells are destroyed,
resulting in a lack of insulin and
hyperglycemia.
Hyperglycemia induces profound osmotic
diuresis, causing water and electrolyte
loss, especially potassium.
The body cannot properly use extracellular
glucose, so starts producing ketones as an
alternate energy source.
Ketosis causes metabolic acidosis.
Metabolic acidosis forces hydrogen ions
into cells, displacing potassium ions that

Pathogenesis cont.
Total-body potassium depletion is present,
but serum potassium levels may be
normal or high because of electrolyte shift
Extreme fluid loss results in clinical shock
In some cases, hyperglycemia and
dehydration predominate, and acidosis is
minimal

Tests

Results

When you suspect DKA, order the

following:
1. FSBS/serum glucose

1. >250 mg/dL rarely >800

mg/dL

- Used serially to follow tx progress

2. Urine or serum ketones

3. ABG

2. High levels confirm dx

3. pH <7.3
pCO2 <40 mmHg

- Used serially to follow tx progress

4. BMP
K+ must be monitored closely
BUN/Cr used to follow tx progress

5. CBC
6. Blood cultures

- confirms dx, reveals severity

4. K+ may be high or normal

- K+ may fall rapidly in tx
- BUN/Cr reveal dehydration

5. Leukocytosis
6. Possible sepsis

Tests cont.

Results cont.

You may choose to order the following

1. Serum Phosphate, Ca,

Mg
2. Amylase/lipase
3. LFTs
Do if c/o abdominal pain

4. EKG
5. CXR
6. Lipids

1. May be decreased.
- May decrease during tx

2. May be elevated in DKA

- May indicate pancreatitis

3. Not usually elevated in DKA

4. Look for peaked T or U
waves
- Look for evidence of
precipitating event

5. Look for precipitating event

6. Likely elevated aid in
ketogenesis

Diagnosis

pH <7.3
Hyperglycemia
Ketonuria
Dehydration

Patient may be asymptomatic, but

should still be treated before
symptoms occur.

Treatment #1: HYDRATION

Hydration with NS. Calculate fluid
deficit. Assume 5-10% dehydration if
patient is acidotic.
Correct over 36-48 hours.
Usually 500-1000mL bolus in first
hour
Children 10-20mL/kg bolus. May use NS,
crystalloid, or LR

Treatment #2: Insulin

Bolus of 0.1 Units/kg IV
Then 0.1 Units/kg/hour IV
Children: no insulin bolus.

0.05-0.1 Units/kg/hour IV

OR (in mild DKA or long transport)

Short-acting insulin
Initial dose 0.3 Units/kg SQ
Then 0.1 Units/kg/hour SQ until glucose <250 mg/dL
Then 0.05 Units/kg/hour SQ until DKA is resolved
Children: no insulin bolus. 0.15 Units/kg/2hours SQ or IM

Caution: Do not reduce serum glucose by more than

80 mg/dL/hour in children, 80-100 mg/dL/hour in adults

Treatment #3: Potassium

20-40 meq/L added to the IV NS
Titrated to serum K+ concentrations
Usually added after assured of urine
output

Other Treatment
Bicarbonate may worsen hypokalemia and intracellular
acidosis and cause cerebral edema.
Used in ICU when pH <6.9

Sodium phosphate is not used routinely.

Tx if: <1 mg/dL OR significant cardiac or respiratory
compromise.

Dextrose 5% if glucose falls too rapidly and when it falls

<250mg/dL. Dont stop insulin until acidosis is corrected.
Caution: If you fail to monitor and replace electrolytes,
rehydrate too fast, or reduce glucose too fast, you may cause
cerebral edema.
If + cerebral edema, do not replace more than 75% of fluid deficit
May use mannitol 0.5-1.0 g/kg over 20 minutes

Follow-up
Look for a cause of the DKA
Make sure glucose is well-controlled
at home and patient is educated
regarding DKA.

Non-Ketotic Hyperosmolar
Coma
Hyperosmolar
Hyperglycemic State
Level of consciousness is depressed when plasma osmolality is high
May be precipitated by concomitant use of certain quinolone
antibiotics in patients with diabetes taking certain oral
hypoglycemic agents

Markedly elevated plasma osmolality

Severe hyperglycemia >600 mg/dL, may exceed 1000 mg/dL
No significant ketonuria/ketonemia
No significant acidosis, pH >7.3 and bicarbonate >15meq/L
Usually occurs in elderly patients who often have undiagnosed DM2
Thromboembolic complications are common
Insulin requirement is less than that for DKA
Requires ICU monitoring

References
David Toth MD et al. Gestational
Diabetes. First Consult . 29 January
2010
Dennis Saver MD et al. Diabetic
Ketoacidosis. First Consult. 27 April
2010.
Abbas E. Kitabchi MD, PhD et al.
Clinical features and diagnosis of
diabetic ketoacidosis and
hyperosmolar hyperglycemic state in