Insulin Therapy & Inpatient Glycemic Control

Insulin preparations and their hazards

Mimicking physiology. Normal secretion has two components: a steady basal output that restrains hepatic glucose production overnight and between meals, and prandial bursts that clear ingested carbohydrate. Regimens copy this with a long-acting or intermediate basal insulin and a rapid-acting or regular mealtime insulin.

Adverse effects. Hypoglycemia is the most important. Weight gain follows reduced glycosuria and insulin's anabolic effects. Repeated injection into one site causes lipohypertrophy, which makes absorption delayed and erratic, so sites are rotated and lumps avoided. Insulin shifts potassium into cells and can cause hypokalemia, most dangerously during IV infusion in DKA. Because the kidney clears insulin, requirements fall and hypoglycemia becomes likelier as GFR declines. Basal analogs cost more than NPH but cause less nocturnal hypoglycemia.

Outpatient regimens

When type 2 patients need insulin. Insulin is indicated when HbA1c is >10%, glucose is ≥300 mg/dL, or there are catabolic features such as weight loss, polyuria and polydipsia, or ketosis. Once glucotoxicity resolves, many patients can de-escalate to noninsulin therapy. When an injectable is needed without these features, a GLP-1 receptor agonist is generally preferred before insulin.

Starting basal insulin. Begin 10 U/day or 0.1–0.2 U/kg/day (glargine or degludec at a consistent time, or NPH at bedtime) and continue metformin. The dose rises about 2 U every 3 days until fasting glucose reaches 80–130 mg/dL, and falls by 10–20% after any unexplained hypoglycemia.

Intensifying. A high HbA1c despite at-goal fasting glucose points to postprandial hyperglycemia. Overbasalization is suggested by basal doses above about 0.5 U/kg/day, a large bedtime-to-morning glucose fall, or hypoglycemia. Rather than escalating basal further, add a GLP-1 receptor agonist or prandial insulin, starting with 4 U (or 10% of the basal dose) before the largest meal and extending to other meals as needed. Sulfonylureas are stopped once prandial insulin starts because hypoglycemia is additive; metformin continues.

Type 1 diabetes. Absolute insulin deficiency requires basal-bolus therapy from diagnosis. The total daily dose is about 0.5 U/kg/day (roughly 0.4–1.0), lower during the honeymoon phase and higher in puberty, pregnancy and acute illness. About half is basal insulin and half rapid-acting insulin divided before meals, matched to carbohydrate intake and supplemented by correction doses. Delivery is by multiple daily injections or an insulin pump, ideally with continuous glucose monitoring.

Basal insulin is never omitted in type 1 diabetes, even when NPO or vomiting: reduce it, do not stop it. Pumps hold only rapid-acting insulin with no subcutaneous depot, so a kinked catheter or pump failure can cause DKA within hours.

Sick days. Continue basal insulin, check glucose every few hours and ketones when glucose is high, keep drinking fluids, and give correction doses; persistent vomiting or rising ketones need urgent evaluation.

Troubleshooting morning hyperglycemia

The 3 AM glucose. A high fasting glucose on insulin may reflect the dawn phenomenon, the Somogyi effect, or evening insulin that simply wanes before morning. A 3 AM fingerstick or a CGM tracing separates them. Waning insulin, with glucose climbing steadily from bedtime, is managed like the dawn phenomenon.

Raising the evening dose in a patient with the Somogyi effect deepens the nocturnal lows, so check overnight glucose before increasing basal insulin for fasting hyperglycemia.

Inpatient glycemic control

Targets. Insulin is started for persistent glucose ≥180 mg/dL, aiming for 140–180 mg/dL in most ICU and ward patients. Tight control (80–110 mg/dL) increased hypoglycemia and mortality in critically ill patients in the NICE-SUGAR trial. An HbA1c is drawn on admission if none was done in the prior 3 months, separating undiagnosed diabetes from stress hyperglycemia.

ICU. Critically ill patients with persistent hyperglycemia receive a protocol-driven IV regular insulin infusion with frequent glucose checks.

Ward patients. Scheduled basal-bolus insulin (basal + prandial + correction) is standard for patients who are eating, typically starting at 0.3–0.5 U/kg/day with half as basal and lower doses for older adults, CKD or poor intake. Sliding-scale insulin alone treats hyperglycemia only after it occurs, produces swings between highs and lows, and is discouraged. Oral agents are usually held: metformin for AKI, contrast and lactic acidosis risk; SGLT2 inhibitors for volume depletion and ketoacidosis; sulfonylureas for hypoglycemia with unpredictable intake.

Not eating or tube-fed. NPO or poorly eating patients receive basal plus correction insulin, with prandial doses held or given right after a meal in proportion to intake. Glucose is checked before meals and at bedtime when eating and every 4–6 h when NPO. Continuous enteral feeding is covered with basal insulin plus scheduled regular insulin every 6 h, and a dextrose infusion is started if feeds stop unexpectedly.

Surgery, steroids and transitions

Perioperative care. Before surgery or a fasting procedure, give about 75–80% of the usual long-acting basal dose (or about half the NPH dose) the evening before or morning of, hold oral agents and prandial insulin that day, and use correction insulin to keep glucose at 100–180 mg/dL around surgery. Metformin is held on the day of surgery. SGLT2 inhibitors are stopped 3 days beforehand (4 days for ertugliflozin) because fasting, stress and lower insulin doses can precipitate euglycemic DKA, an anion-gap ketoacidosis with glucose often below 250 mg/dL that is treated with insulin plus dextrose-containing fluids.

Glucocorticoid-induced hyperglycemia. A single morning prednisone dose drives hyperglycemia in the afternoon and evening that wanes overnight, so fasting glucose can be near normal while pre-lunch and pre-dinner values soar; screen with those later readings. NPH given in the morning with the steroid matches this profile, at about 0.1 U/kg for each 10 mg of prednisone up to 0.4 U/kg, and is tapered alongside the steroid to prevent hypoglycemia. Dexamethasone or divided steroid doses cause sustained hyperglycemia that needs longer-acting basal coverage.

From infusion to subcutaneous insulin. IV regular insulin has a half-life of minutes, so any gap before subcutaneous insulin takes effect invites rebound hyperglycemia or recurrent DKA.

Special populations. Insulin is the preferred drug for pregestational and gestational diabetes; requirements rise through the second and third trimesters as placental hormones increase insulin resistance, then fall sharply after delivery. In CKD, reduced insulin clearance lowers requirements. Frail older adults do best with simple regimens, often basal insulin alone, with relaxed targets and no sliding scales.