How should I emergently treat an 82‑year‑old woman with type 1 diabetes, prior stroke, severe hypertension (195/102 mmHg), hypoglycemia (glucose 50 mg/dL), hypokalemia (K⁺ 2.7 mmol/L), metabolic acidosis (bicarbonate 10 mmol/L) and hyperammonemia (34 µmol/L)?

Medical Advisory BoardAll articles are reviewed for accuracy by our Medical Advisory Board
Educational purpose only • Exercise caution as content is pending human review
Article Review Status
Submitted
Under Review
Approved

Last updated: February 27, 2026View editorial policy

Personalize

Help us tailor your experience

Which best describes you? Your choice helps us use language that's most understandable for you.

Emergency Management of Severe Metabolic Crisis in Type 1 Diabetes

Immediate Life-Threatening Priorities (First 30 Minutes)

This patient presents with diabetic ketoacidosis (DKA), severe hypokalemia, profound metabolic acidosis, and hypoglycemia—a constellation requiring simultaneous correction to prevent cardiac arrest and cerebral edema.

1. Airway and Hemodynamic Stabilization

  • Secure airway if Glasgow Coma Scale <8 or unable to protect airway; provide supplemental oxygen to maintain saturation ≥94% 1.
  • Establish two large-bore IV lines for simultaneous fluid resuscitation and electrolyte replacement 2, 3.
  • Place on continuous cardiac monitoring given severe hypokalemia (K⁺ 2.7 mEq/L) which predisposes to fatal arrhythmias 4.

2. Correct Life-Threatening Hypoglycemia FIRST

  • Administer 25 grams IV dextrose (50 mL of D50W) immediately for glucose 50 mg/dL to prevent seizures and neurologic injury 1.
  • Recheck glucose in 15 minutes; repeat 15 g dextrose if <70 mg/dL 1.
  • Do NOT start insulin until glucose >200 mg/dL and potassium >3.3 mEq/L to avoid precipitating cardiac arrest 4, 2.

3. Aggressive Potassium Repletion (Critical—Delays Insulin)

  • Withhold insulin completely until serum potassium ≥3.3 mEq/L because insulin drives potassium intracellularly and can cause fatal arrhythmias 4, 2, 3.
  • Start 40 mEq/hour IV potassium chloride (maximum safe peripheral rate) via central line if available; peripheral administration requires dilution to ≤10 mEq/100 mL 4.
  • Recheck potassium every 1–2 hours initially; expect to administer 400–800 mEq in first 24 hours given profound total-body depletion 4.
  • Once K⁺ reaches 3.3–5.0 mEq/L, reduce to 20–30 mEq/hour and continue aggressive replacement 2, 3.

Fluid Resuscitation (Simultaneous with Potassium)

Initial Bolus

  • Administer 1–2 liters 0.9% normal saline over first hour to restore circulating volume and improve tissue perfusion 2, 3.
  • Reassess hemodynamics; if hypotensive (BP 195/102 suggests hypertensive emergency, not shock), reduce rate to 250–500 mL/hour 2, 3.

Maintenance Fluids

  • After initial bolus, switch to 0.45% saline at 250–500 mL/hour to replace free water deficit while avoiding rapid osmolality shifts 2, 3.
  • When glucose falls to 200–250 mg/dL, add 5% dextrose to IV fluids (D5-0.45% saline) to prevent hypoglycemia while continuing insulin for ketoacidosis resolution 2, 3.
  • Target total fluid replacement of 4–6 liters over first 12–24 hours depending on degree of dehydration 2, 3.

Insulin Therapy (Only After K⁺ ≥3.3 mEq/L and Glucose >200 mg/dL)

Initiation

  • Start continuous IV regular insulin at 0.1 units/kg/hour (approximately 5–7 units/hour for 70 kg adult) 2, 3.
  • Do NOT give IV bolus in this patient given initial hypoglycemia and severe hypokalemia 2, 3.

Titration

  • Target glucose decline of 50–75 mg/dL per hour; if glucose not falling adequately, increase insulin infusion by 1 unit/hour every hour 2, 3.
  • Once glucose reaches 200–250 mg/dL, reduce insulin to 0.05 units/kg/hour and add dextrose to IV fluids 2, 3.
  • Continue insulin infusion until anion gap closes (<12 mEq/L) and bicarbonate >15 mEq/L, not just until glucose normalizes 2, 3.

Bicarbonate Therapy (Controversial—Use Cautiously)

Indications

  • Consider sodium bicarbonate only if pH <6.9 to prevent cardiovascular collapse 1, 5, 2.
  • Administer 100 mEq sodium bicarbonate in 400 mL sterile water over 2 hours if pH <6.9 5, 2.
  • Avoid bicarbonate if pH ≥6.9 because it increases risk of hypokalemia, paradoxical CNS acidosis, and cerebral edema 1, 2.

Monitoring

  • Recheck arterial blood gas 2 hours after bicarbonate; repeat dose if pH remains <6.9 5, 2.
  • Increase potassium replacement by 10–20 mEq/hour during bicarbonate therapy because alkalinization drives potassium into cells 5, 2.

Metabolic Acidosis Management

Anion Gap Calculation

  • Anion gap = Na⁺ – (Cl⁻ + HCO₃⁻) = 195 – (unknown Cl⁻ + 10) 2, 3.
  • Elevated anion gap confirms ketoacidosis; check serum/urine ketones (β-hydroxybutyrate preferred) 2, 3.

Resolution Criteria

  • DKA resolved when: glucose <200 mg/dL, bicarbonate ≥15 mEq/L, pH >7.3, and anion gap <12 mEq/L 2, 3.
  • Typically requires 12–24 hours of continuous insulin infusion 2, 3.

Hypertensive Emergency Management

Blood Pressure Control

  • Do NOT aggressively lower BP initially because cerebral perfusion may be impaired by severe acidosis and hyperosmolality 1.
  • If systolic BP remains >220 mmHg or diastolic >120 mmHg after fluid resuscitation, use short-acting IV agents (labetalol 10–20 mg IV bolus or nicardipine 5 mg/hour infusion) 1.
  • Avoid rapid BP reduction >25% in first hour to prevent cerebral ischemia 1.

Hyperammonemia Evaluation

Significance

  • Ammonia 34 µmol/L is mildly elevated (normal <35 µmol/L) and likely reflects hepatic stress from DKA 2.
  • Check liver function tests (AST, ALT, bilirubin) to exclude acute hepatic injury 2.
  • Ammonia typically normalizes with DKA resolution; no specific therapy needed unless >100 µmol/L 2.

Monitoring Protocol

Hourly

  • Capillary glucose, vital signs, neurologic status, urine output 2, 3.

Every 2 Hours

  • Serum potassium, sodium, chloride, bicarbonate, anion gap 2, 3.
  • Arterial or venous blood gas if pH <7.0 initially 2, 3.

Every 4 Hours

  • Complete metabolic panel, magnesium, phosphate 2, 3.

Transition to Subcutaneous Insulin

Timing

  • When DKA resolved (pH >7.3, bicarbonate >15 mEq/L, anion gap <12 mEq/L, patient able to eat) 2, 3.

Protocol

  • Give subcutaneous basal insulin (glargine 0.25 units/kg) 2–4 hours before stopping IV insulin to prevent rebound ketoacidosis 2, 3.
  • Start rapid-acting insulin 0.1 units/kg before meals 2, 3.
  • Continue IV insulin for 1–2 hours after first subcutaneous dose to ensure overlap 2, 3.

Critical Pitfalls to Avoid

  • Never start insulin before correcting hypokalemia (K⁺ <3.3 mEq/L)—this causes cardiac arrest 4, 2.
  • Never stop insulin when glucose normalizes—continue until anion gap closes to prevent rebound ketoacidosis 2, 3.
  • Never give bicarbonate if pH ≥6.9—increases cerebral edema risk 1, 2.
  • Never correct hyperglycemia faster than 75 mg/dL per hour—precipitates cerebral edema 2, 3.
  • Never use metformin in DKA—causes lactic acidosis in setting of tissue hypoperfusion 6.

Expected Outcomes

  • With aggressive potassium repletion (400–800 mEq in 24 hours), serum K⁺ normalizes in 8–12 hours 4.
  • DKA resolution typically occurs in 12–24 hours with continuous insulin infusion 2, 3.
  • Mortality in DKA is <1% with appropriate management but approaches 10% if hypokalemia or cerebral edema develop 2.

References

Guideline

Guideline Directed Topic Overview

Dr.Oracle Medical Advisory Board & Editors, 2025

Research

Profound hypokalemia in diabetic ketoacidosis: a therapeutic challenge.

Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists, 2005

Related Questions

What is the appropriate insulin dose for a 112 kg patient with hyperglycemia (glucose 297) in the Emergency Department (ED)?
What is the difference between diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS)?
What is the appropriate management for a patient presenting with severe dehydration, hyperglycemia, and significant ketonuria, accompanied by symptoms of nausea, vomiting, and chest pain?
At what fasting plasma glucose level, and with which clinical features (e.g., diabetic ketoacidosis, hyperosmolar hyperglycemic state, severe dehydration, electrolyte disturbances, acute infection, myocardial infarction, stroke, pregnancy), should a patient be hospitalized rather than managed with outpatient oral antidiabetic agents?
What are the key biochemistry parameters to differentiate between diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) in patients with suspected hyperglycemia?
Will Keflex (cephalexin) cover Klebsiella from a positive wound culture?
What is the recommended diagnostic and management protocol for a 3.7 cm hepatic lesion?
How should peripheral neuropathic pain be managed in a maintenance hemodialysis patient already taking duloxetine 20 mg daily and gabapentin 100 mg nightly?
Should music therapy be used as an adjunctive non‑pharmacologic intervention for adult ischemic or hemorrhagic stroke survivors in any recovery phase who have motor weakness, gait disturbance, speech/language deficits, or mood changes, and what are the recommended treatment parameters?
What is the volume (mL) of the Ciprodex (ciprofloxacin 0.3%/dexamethasone 0.1%) otic suspension bottle?
How should isolated systolic hypertension be managed?

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

Have a follow-up question?

Our Medical A.I. is used by practicing medical doctors at top research institutions around the world. Ask any follow up question and get world-class guideline-backed answers instantly.