Hypoglycemia in adults
Hypoglycemia is a plasma glucose below 70 mg/dL, most often a complication of insulin or sulfonylurea therapy for diabetes, and in a person without diabetes it requires a Whipple triad-based evaluation for insulinoma or another endogenous cause. An alert patient is treated with 15 to 20 g of fast-acting oral carbohydrate, while a patient unable to swallow safely receives intramuscular glucagon 1 mg or intravenous dextrose 50% 25 g.
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What this article covers
- Overview
A glucose value, not a single disease: biochemically defined as plasma glucose below 70 mg/dL (3.9 mmol/L), with a value below 54 mg/dL (3.0 mmol/L) considered clinically significant and any episode…
- Epidemiology
A rate-limiting complication of intensive glycemic control: a major barrier to achieving glycemic targets in patients on insulin or secretagogues.
- Risk factors
Insulin or insulin secretagogue therapy: the dominant risk factor; risk rises with more intensive regimens and tighter targets.
- Pathophysiology
Falling glucose triggers a counterregulatory cascade: as glucose declines, insulin secretion is suppressed, then glucagon, epinephrine, norepinephrine, cortisol, and growth hormone are released to restore euglycemia.
- Clinical features
Hyperadrenergic (autonomic) symptoms: sweating, tremor, anxiety, palpitations, tachycardia; typically the first symptoms noticed and prompt self-treatment while awareness is intact.
- Differential diagnosis
Insulin or sulfonylurea/meglitinide effect (in diabetes): by far the most common cause; a temporal relationship to dosing, a missed meal, or exertion, unlike the unprovoked pattern of endogenous hyperinsulinism, points here first.
- Diagnosis
The clinching basis differs by clinical setting.
- Management
First, in an alert patient who can safely swallow, give 15 to 20 g of a fast-acting carbohydrate orally (glucose tablets or gel, juice, or regular soda), then recheck glucose 15 to 20 minutes later.
- Complications
Seizure, coma, and death: the most severe outcomes of uncorrected neuroglycopenia.
- Prognosis
Excellent for isolated, promptly treated episodes: glucose correction reverses symptoms without lasting sequelae in most patients.
- Prevention
Individualize glycemic targets to avoid severe hypoglycemia: resolving recurrent severe hypoglycemia takes precedence over reaching a hemoglobin A1c goal.
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- Type 2 diabetes mellitus
Type 2 diabetes is hyperglycemia from insulin resistance with progressive relative insulin deficiency, diagnosed by a hemoglobin A1c of 6.5% or higher, a fasting glucose of 126 mg/dL or higher, or a 2-hour oral glucose tolerance test value of 200 mg/dL or higher. First-line treatment is lifestyle modification plus metformin, with an SGLT2 inhibitor or GLP-1 receptor agonist added early for patients with atherosclerotic disease, kidney disease, or heart failure.
- Insulin therapy in diabetes mellitus
Insulin therapy replaces or supplements endogenous insulin to control hyperglycemia, and is lifelong and mandatory in type 1 diabetes because of absolute beta-cell failure, while in type 2 diabetes it is added when oral and noninjectable agents fail to reach glycemic goals. First-line therapy is a basal-bolus regimen started at 0.4-1.0 units/kg/day in type 1 diabetes, or basal insulin glargine 10 units/day (or 0.1-0.2 units/kg/day) in type 2 diabetes, titrated to a fasting glucose target.
- Insulin autoimmune syndrome
Insulin autoimmune syndrome is spontaneous hyperinsulinemic hypoglycemia in a person without prior insulin exposure, caused by high-titer autoantibodies that bind endogenous insulin and release it unpredictably, or by antibodies that directly activate the insulin receptor. First-line treatment is dietary, with small frequent low-glycemic-index meals and avoidance of any culprit drug; refractory or severe recurrent hypoglycemia is treated with prednisone 30-60 mg orally once daily, tapered over 1 to 3 months.