Reference — Endocrine
Endocrine Crisis Management Reference
DKA, HHS, thyroid storm, adrenal crisis, and severe hypoglycemia — triggers, key labs, priority interventions, do-not actions, and resolution criteria at a glance.
Educational use only. Endocrine crises are life-threatening emergencies. Always follow institutional protocols, provider orders, and involve the rapid response or endocrinology team as appropriate. This material supports nursing education and exam review. It is not medical advice and is not a substitute for clinical judgment, institutional policy, or medical direction. Always follow facility protocols and current provider orders.
Diabetic Ketoacidosis (DKA)
Typical patient: Type 1 DM; can occur in Type 2 under severe stress
| Trigger | Missed insulin (most common in known T1DM), infection/illness, new diagnosis of T1DM, excessive alcohol, stress |
| Key Labs | Glucose > 250 mg/dL, pH < 7.3, HCO₃ < 18 mEq/L, positive ketones (urine or serum), elevated anion gap (> 12), often hypokalemia once treatment begins, BUN/Cr elevated (dehydration) |
| First Action | IV Normal Saline (NS) 1 L/hr for first 1–2 hours — fluid resuscitation BEFORE or simultaneously with insulin |
| Insulin Notes | IV Regular insulin drip ONLY (0.1 units/kg/hr); add dextrose to IV fluids when glucose reaches 200–250 mg/dL (continue insulin to clear ketones); DO NOT stop insulin when glucose normalizes |
| Potassium / Electrolytes | CHECK potassium before starting insulin. If K⁺ < 3.5: replace potassium FIRST, delay insulin (insulin drives K⁺ into cells → can cause fatal hypokalemia). If K⁺ 3.5–5.5: add K⁺ to fluids. If K⁺ > 5.5: hold potassium replacement, give insulin. |
| Do NOT | Do NOT give insulin without checking K⁺ first. Do NOT stop insulin when glucose normalizes (ketones may still be present). Do NOT use D50W to treat glucose drop — use D5NS instead. |
| Resolution | pH > 7.3, HCO₃ > 18 mEq/L, anion gap normalized, patient tolerating oral intake → transition to SQ insulin 2h before stopping drip |
Hyperosmolar Hyperglycemic State (HHS)
Typical patient: Type 2 DM, elderly, often undiagnosed diabetes; develops over days to weeks
| Trigger | Infection (most common), inadequate fluid intake, medications (diuretics, steroids), illness in Type 2 DM |
| Key Labs | Glucose > 600 mg/dL (often 800–2000), serum osmolality > 320 mOsm/kg (often > 350), minimal or no ketones, pH normal (no significant acidosis), severely elevated BUN/Cr |
| First Action | IV fluid resuscitation is the priority — patients are severely dehydrated (may be 8–10+ liters deficit). NS first, then transition to ½NS based on sodium and clinical status. |
| Insulin Notes | Insulin given at lower rates than DKA (fluids do much of the work). Glucose drops primarily from fluid resuscitation. Start insulin after initial fluid bolus. Add dextrose when glucose approaches 300 mg/dL. |
| Potassium / Electrolytes | Same rule as DKA: check K⁺ before insulin. HHS patients often have normal-to-low K⁺ (not as low as DKA typically) — but still monitor closely as insulin causes intracellular shift. |
| Do NOT | Do NOT lower glucose or osmolality too rapidly — rapid correction can cause cerebral edema. Lower glucose by no more than 50–75 mg/dL per hour. Monitor neuro status continuously. |
| Resolution | Glucose < 300 mg/dL, osmolality normalized, mental status improved, adequate oral intake → SQ insulin transition |
Thyroid Storm (Thyrotoxic Crisis)
Typical patient: Known hyperthyroidism (often Graves') with physiologic stressor; occasionally first presentation
| Trigger | Surgery on or adjacent to thyroid, iodine load (contrast), abrupt antithyroid drug discontinuation, infection, labor/delivery, trauma in patient with uncontrolled hyperthyroidism |
| Key Labs | TSH suppressed (near undetectable), markedly elevated free T3 and free T4; elevated LFTs; tachycardia/A-fib on ECG; Burch-Wartofsky score ≥ 45 = thyroid storm |
| First Action | Beta-blocker IV (propranolol) — controls tachycardia and inhibits T4→T3 conversion. Give IMMEDIATELY. |
| Medication Sequence | PTU FIRST → then potassium iodide 1 hour later (never give iodide first — provides substrate for hormone synthesis). Corticosteroids (hydrocortisone) reduce T4→T3 conversion and treat relative adrenal insufficiency. |
| Do NOT | Do NOT give aspirin for fever — aspirin displaces T4 from binding proteins, worsening thyrotoxicosis. Use acetaminophen ONLY. Do NOT give potassium iodide before PTU. |
| Resolution | Heart rate controlled, temperature trending down, mental status improving — transition to oral antithyroid drugs; monitor for post-storm hypothyroidism |
Adrenal (Addisonian) Crisis
Typical patient: Patient on chronic corticosteroids who vomits pills or does not increase dose during illness; known Addison's disease; post-adrenalectomy
| Trigger | Illness/infection in patient on chronic steroids without dose increase, abrupt corticosteroid discontinuation, physiologic stress in Addison's disease, bilateral adrenal hemorrhage (Waterhouse-Friderichsen) |
| Key Labs | Very low cortisol, very high ACTH (if primary), hyponatremia, hyperkalemia, hypoglycemia, eosinophilia, elevated BUN (dehydration); hypotension unresponsive to fluids |
| First Action | IV Hydrocortisone 100 mg IV bolus IMMEDIATELY — do not wait for lab confirmation if clinically suspected. Treat first. |
| Insulin Notes | N/A — may need dextrose (hypoglycemia is common); D5NS is the preferred IV fluid |
| Potassium / Electrolytes | Monitor K⁺ — hyperkalemia from aldosterone deficiency; will correct with hydrocortisone (which has some mineralocorticoid activity) and IV fluid. After crisis stabilized, add fludrocortisone for primary adrenal insufficiency. |
| Do NOT | Do NOT delay hydrocortisone while waiting for lab results — crisis can be fatal within hours. Do NOT abruptly stop steroids in stable patient (adrenal crisis trigger). Steroid dose does NOT need to be weaned slowly during treatment of crisis. |
| Resolution | BP stabilized, glucose normalized, alert — taper IV hydrocortisone; transition to oral maintenance plus fludrocortisone; educate on stress dosing, medical alert bracelet |
Severe Hypoglycemia
Typical patient: Any diabetic patient on insulin or sulfonylureas; can occur in non-diabetic patients (insulinoma, liver failure, sepsis)
| Trigger | Insulin overdose, sulfonylurea excess, missed meal, extreme exercise, alcohol, renal failure (reduced insulin clearance), NPO without insulin adjustment |
| Key Labs | Glucose < 54 mg/dL (Level 2); severe = any glucose level with loss of consciousness, seizure, or requires another person to treat. Also: check for other causes (ketones if Type 1 simultaneously has DKA + hypoglycemia from treatment) |
| First Action | If IV access: D50W 25g (50 mL) IV immediately. If no IV access: Glucagon 1 mg IM or intranasal (Baqsimi). Recheck glucose in 15 minutes. |
| Insulin Notes | Identify and address the cause. Reduce insulin dose per provider order after any severe hypoglycemia event. DO NOT skip future insulin doses without order — adjust, don't eliminate. |
| Do NOT | Do NOT give oral glucose to unconscious patient — aspiration risk. Do NOT assume glucagon is always effective — ineffective in malnourished, liver failure, or glycogen-depleted patients (use D50W). Do NOT leave patient alone until glucose > 80 mg/dL and patient is alert. |
| Resolution | Glucose > 80 mg/dL, patient alert, able to swallow safely → provide carbohydrate + protein snack if meal > 1h away; document; notify provider; review insulin regimen |
Related Resources
Standards & sources
Fact-checked Jun 20, 2026This page is written to align with American Diabetes Association (ADA) Standards of Care · American Association of Clinical Endocrinology (AACE). It is an educational summary, not a citation of any single document — always verify specific doses, values, and protocols against current guidelines and your facility policy. How we source content →