Diabetic Ketoacidosis and Hyperglycemia

Diabetic Ketoacidosis
and Hyperglycemia
Valerie Robinson, D.O.
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 ß-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
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, Charcot’s 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
• May be the initial presentation of diabetes
• 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)
Abdominal pain (ileus or delayed emptying)
Altered consciousness
Kussmaul breathing (compensatory hyperventilation)
• Pancreatic islet cells are destroyed, resulting in a lack
of insulin and hyperglycemia.
• Hyperglycemia induces profound osmotic diuresis,
causing water and electrolyte loss, especially
• The body cannot properly use extracellular glucose,
so starts producing ketones as an alternate energy
• Ketosis causes metabolic acidosis.
• Metabolic acidosis forces hydrogen ions into cells,
displacing potassium ions that are lost through urine
and vomiting. Increased anion gap: Usu. >20meq/L
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
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
- 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
2. High levels confirm dx
3. pH <7.3 pCO2 <40 mmHg
- 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 1. May be decreased.
- May decrease during tx
2. Amylase/lipase
2. May be elevated in DKA
- May indicate pancreatitis
3. LFTs
3. Not usually elevated in DKA
Do if c/o abdominal pain
4. EKG
4. Look for peaked T or U waves
- Look for evidence of precipitating event
5. CXR
6. Lipids
5. Look for precipitating event
6. Likely elevated – aid in ketogenesis
pH <7.3
• 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
• 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
• Dextrose 5% if glucose falls too rapidly and when it falls
<250mg/dL. Don’t 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
• 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
• 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
adults. UpToDate. 25 June 2012.

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