Hepatic Failure/GI/Endocrine Emergencies
vii.
Continuous insulin infusions should be continued until ketoacidosis resolves in DKA and
abnormal serum osmolality and mental status in HHS resolve; then, change to subcutaneous
insulin.
| (a) | Criteria for resolution of ketoacidosis include a BG less than 200 mg/dL and two of the |
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following: a serum bicarbonate concentration of 15 mEq/L or greater, a venous pH greater
than 7.3, and a normalization of anion gap. Per guidelines, anion gap should be 12 mEq/L
or less, but normal range may vary by institution.
| (b) | For patients with new insulin requirement, doses of 0.5–0.8 units/kg of subcutaneous |
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insulin per day can be used with a basal (glargine or detemir) and bolus (lispro, aspart,
or glulisine). For patients previously on subcutaneous insulin therapy, outpatient insulin
requirement can be used to guide dosing; weight-based dosing may be insufficient for
those who have high baseline requirements. There should be an overlap of 1–2 hours
between administration of subcutaneous insulin and discontinuation of intravenous
insulin infusion.
| (c) | Subcutaneous insulin can be used in patients with mild or moderate DKA or HHS but |
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have not been evaluated in patients with severe disease.
| (1) | Basal insulin is started at a dose of 0.15–0.3 units/kg and repeated every 12–24 hours. |
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| (2) | An initial bolus of 0.2 units/kg of rapid acting insulin is also given. Subsequent doses |
of rapid acting insulin are repeated every 2–4 hours until DKA has resolved.
| d. | Potassium should be replaced aggressively (assuming adequate renal function) with a goal serum |
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potassium of 4–5 mEq/L.
Patients with initial serum potassium less than 3.3 mEq/L should have insulin withheld and
potassium administered until their serum potassium is above 3.3 mEq/L.
ii.
Patients with serum potassium of 3.3–5.2 mEq/L should have 20–30 mEq of potassium added
to each liter of intravenous fluid administered.
iii.
Patients with initial serum potassium greater than 5.2 mEq/L should not receive potassium,
but they should be monitored closely (with potassium administered if the patient’s serum
falls below 5 mEq/L). Of importance, patients with DKA and initial hyperkalemia should
not receive therapy directed toward total body potassium removal (e.g., sodium polystyrene
sulfonate or furosemide). The patient’s serum potassium will typically decrease as insulin is
administered.
Intravenous sodium bicarbonate should not be administered routinely.
Acidemia will typically quickly correct as ketosis is resolved, and bicarbonate may have
deleterious effects (e.g., hypokalemia).
ii.
Studies of patients with DKA with a pH of 6.9 or greater have not supported a benefit with
sodium bicarbonate administration.
iii.
A recent study of sodium bicarbonate in ICU patients showed a potential mortality benefit in
patients with acute kidney injury. However, this study excluded patients with ketoacidosis.
iv.
Guidelines recommend administering bicarbonate in the setting of severe metabolic acidosis
(pH less than 7).
| (a) | Suggested dosing regimen is 100 mL of 8.4% sodium bicarbonate solution in 400 mL of |
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sterile water every 2 hours to achieve pH greater than 7. Phosphorus repletion should be
initiated in patients with serum phosphate below 1 mg/dL or in those with severe cardiac
or respiratory dysfunction associated with hypophosphatemia.
Clinical presentation
Because hyperglycemia is so prevalent in critically ill patients, there is no specific clinical
presentation.