1. Diabetic Ketoacidosis and Hyperglycemia
Valerie Robinson, D.O.

2. 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 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 death.

3. 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

4. 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

5. 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)

6. 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 are lost through urine and vomiting. Increased anion gap: Usu. >20meq/L

7. 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

8. Tests Results When you suspect DKA, order the following:
FSBS/serum glucose
- Used serially to follow tx progress
Urine or serum ketones
ABG
BMP
K+ must be monitored closely
BUN/Cr used to follow tx progress
CBC
Blood cultures
>250 mg/dL rarely >800 mg/dL
High levels confirm dx
pH < pCO2 <40 mmHg
- confirms dx, reveals severity
K+ may be high or normal
- K+ may fall rapidly in tx
- BUN/Cr reveal dehydration
Leukocytosis
Possible sepsis

9. Tests cont. Results cont. Serum Phosphate, Ca, Mg Amylase/lipase LFTs
You may choose to order the following
Serum Phosphate, Ca, Mg
Amylase/lipase
LFTs
Do if c/o abdominal pain
EKG
CXR
Lipids
May be decreased.
- May decrease during tx
May be elevated in DKA
- May indicate pancreatitis
Not usually elevated in DKA
Look for peaked T or U waves
- Look for evidence of precipitating event
Look for precipitating event
Likely elevated – aid in ketogenesis

10. Diagnosis pH <7.3 Hyperglycemia Ketonuria Dehydration
Patient may be asymptomatic, but should still be treated before symptoms occur.

11. Treatment #1: HYDRATION
Hydration with NS. Calculate fluid deficit. Assume 5-10% dehydration if patient is acidotic.
Correct over hours.
Usually mL bolus in first hour
Children 10-20mL/kg bolus. May use NS, crystalloid, or LR

12. Treatment #2: Insulin Bolus of 0.1 Units/kg IV
Then 0.1 Units/kg/hour IV
Children: no insulin bolus 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 Units/kg/2hours SQ or IM
Caution: Do not reduce serum glucose by more than
80 mg/dL/hour in children, mg/dL/hour in adults

13. Treatment #3: Potassium
20-40 meq/L added to the IV NS
Titrated to serum K+ concentrations
Usually added after assured of urine output

14. 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. 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 g/kg over 20 minutes

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

16. 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

17. 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 adults. UpToDate. 25 June 2012.