Diabetes and Metabolic Emergencies

Learning objectives

After completing this chapter, you should be able to distinguish pregestational diabetes from gestational diabetes; recognize diabetic ketoacidosis at lower glucose levels; interpret ketones, anion gap, bicarbonate, pH, and potassium; sequence DKA treatment safely; manage hypoglycemia; recognize hyperosmolar and starvation states; anticipate fetal effects; and make appropriate transport decisions.

Opening transport scenario

A 25-year-old patient at 31 weeks with type 1 diabetes presents after vomiting and missed insulin. Glucose is 238 mg/dL, heart rate 128/min, respiratory rate 30/min, bicarbonate 13 mEq/L, anion gap 22, and beta-hydroxybutyrate is elevated. Fetal heart rate is 175/min with minimal variability. Because the glucose is not dramatically elevated, the initial team questions DKA. The transport clinician must recognize that pregnancy is ketogenic and DKA may occur at lower glucose concentrations.

1. Diabetes encountered in maternal transport

2. Why pregnancy changes metabolic emergencies

Pregnancy increases insulin resistance, accelerates starvation physiology, and promotes lipolysis and ketone production. Placental hormones, fetal glucose use, vomiting, reduced intake, infection, beta-agonists, corticosteroids, and insulin interruption can cause rapid deterioration. The American Diabetes Association notes that pregnancy is a ketogenic state and DKA may occur at lower glucose levels than in nonpregnant adults.

3. Recognizing DKA and euglycemic DKA

DKA is diagnosed by the combination of diabetes or hyperglycemia, elevated ketones, and metabolic acidosis. Glucose alone is not sufficient. In pregnancy, euglycemic or modestly hyperglycemic DKA is especially important.

4. Common precipitants

• Insulin omission, pump malfunction, empty reservoir, kinked cannula, or device failure.
• Vomiting, hyperemesis, dehydration, or prolonged fasting.
• Infection, sepsis, pyelonephritis, pneumonia, or intra-amniotic infection.
• Antenatal corticosteroids and beta-agonist therapy.
• New diabetes, myocardial ischemia, pancreatitis, thyroid disease, or medication effect.
• SGLT2 inhibitors in patients who became pregnant while taking them.

5. DKA treatment sequence

Effective treatment restores perfusion, replaces potassium and other electrolytes, stops ketogenesis with insulin, adds dextrose when needed so insulin can continue, and corrects the precipitating cause. The treatment sequence matters.

1. Airway and monitoring: assess work of breathing and mental status; apply ECG, frequent BP, SpO₂, glucose, and fetal monitoring when viable.
2. Balanced fluid resuscitation: begin ordered isotonic fluid while reassessing lung findings, urine output, sodium, perfusion, and cardiac/renal status.
3. Potassium decision: if potassium is dangerously low, replace potassium before insulin. If normal or high, monitor closely because insulin and correction of acidosis will drive potassium intracellularly.
4. Insulin infusion: use the institutional IV insulin protocol after potassium safety is addressed; avoid unverified pump continuation during unstable DKA.
5. Add dextrose: when glucose falls to the protocol threshold, add dextrose so insulin can continue until the anion gap and ketosis resolve.
6. Treat cause: cultures, antibiotics, antiemetics, device replacement, or other cause-directed care.

Why potassium can fall abruptly

Insulin deficiency and acidosis move potassium out of cells, while osmotic diuresis depletes total body stores. Once insulin begins and acidosis improves, serum potassium may drop rapidly. Continuous ECG and frequent laboratory reassessment are essential.

6. Fetal assessment and delivery decisions

Fetal tachycardia, minimal variability, or decelerations may occur during maternal dehydration and acidosis. Correct maternal physiology, position appropriately, monitor continuously when feasible, and involve obstetrics early. Delivery during uncontrolled maternal DKA may increase risk and is usually reserved for a separate obstetric indication or persistent fetal compromise despite maternal stabilization.

7. Hypoglycemia

Hypoglycemia may result from insulin, poor intake, vomiting, increased activity, renal dysfunction, or delivery-related changes in insulin requirement. Symptoms include sweating, tremor, palpitations, confusion, seizure, focal neurologic deficit, and coma.

• Give oral carbohydrate only when the patient can safely swallow.
• Use IV dextrose or glucagon according to severity, access, and protocol.
• Recheck glucose and provide sustained carbohydrate when recurrence is likely.
• Identify long-acting insulin, sulfonylurea, pump settings, renal disease, and decreased intake.
• After treatment, reassess maternal neurologic status and fetal status.

8. HHS, starvation ketoacidosis, and other metabolic disorders

Hyperosmolar hyperglycemic state

HHS is characterized by profound hyperglycemia, hyperosmolality, dehydration, and altered mental status with little or less prominent ketoacidosis. It requires careful fluid, electrolyte, insulin, and cause-directed therapy.

Starvation ketoacidosis

Pregnancy can produce clinically important ketoacidosis after a relatively short period of reduced intake, especially with vomiting or infection. Glucose may be normal or low. Treatment commonly includes dextrose-containing fluid, electrolyte correction, thiamine when malnutrition is possible, and treatment of the trigger; insulin may be needed under specialist direction.

Lactic acidosis and severe electrolyte disorders

Sepsis, shock, seizure, hypoxemia, medication toxicity, renal failure, and hepatic disease may produce acidosis. Do not assume every anion-gap acidosis is DKA. Interpret lactate, ketones, renal function, toxic exposures, and the clinical context.

9. Insulin pumps and continuous glucose monitors

Document the device type, basal rate, last bolus, reservoir volume, insertion site, alarms, and who is managing it. During severe illness, altered mental status, DKA, shock, or a procedure, a controlled IV insulin protocol may be safer than patient-managed pump therapy. CGM values may lag during rapid change or poor perfusion; confirm unexpected values with a validated point-of-care or laboratory test.

10. Transport implementation

• Carry sufficient insulin, dextrose, potassium, pumps, tubing, fluids, and point-of-care supplies for the mission and delays.
• Document exact infusion concentrations, rates, recent changes, and the next laboratory time.
• Trend glucose, potassium, bicarbonate, anion gap, beta-hydroxybutyrate, pH, sodium, urine output, and fetal status.
• Do not transport an unstable patient without a plan for severe hypokalemia, pulmonary edema, cerebral change, or emergent delivery.
• Choose a destination with obstetric, endocrine/critical-care, laboratory, and neonatal capability.

11. Evolving case study

Phase 1: Diagnosis

The patient has elevated beta-hydroxybutyrate and anion-gap acidosis despite glucose 238 mg/dL. The team recognizes pregnancy-associated DKA rather than excluding it.

Phase 2: Treatment

Balanced fluids are started. Potassium is 3.1 mEq/L and replacement begins before insulin. Dextrose is added later so insulin can continue while ketones and gap remain elevated.

Phase 3: Fetal response

As maternal perfusion and acidosis improve, fetal tachycardia resolves and variability improves. The team continues transport to a center with maternal critical care and NICU rather than pursuing delivery solely for the initial tracing.

12. High-yield chapter summary

1. Pregnancy accelerates ketosis and DKA can occur at lower glucose levels.
2. DKA requires ketones and metabolic acidosis; glucose alone does not diagnose or exclude it.
3. Total body potassium is depleted even when serum potassium is normal or high.
4. Severe hypokalemia must be corrected before insulin.
5. Dextrose allows insulin to continue until ketogenesis and the anion gap resolve.
6. Treat the precipitating cause.
7. Fetal abnormalities often improve with maternal resuscitation.
8. Hypoglycemia requires treatment, reassessment, and recurrence prevention.
9. Starvation ketoacidosis can occur after relatively brief fasting in pregnancy.
10. Verify pump and CGM data; unstable DKA generally requires controlled protocol-based therapy.

References

1. International Board of Specialty Certification. Maternal Fetal Transport Microcredential Candidate Handbook. Updated April 2026.
2. American Diabetes Association. Standards of Care in Diabetes—2026: Management of Diabetes in Pregnancy.
3. American Diabetes Association. Hyperglycemic Crises in Adults With Diabetes: Consensus Report.
4. American College of Obstetricians and Gynecologists. Guidance on pregestational and gestational diabetes.
5. Society for Maternal-Fetal Medicine. Maternal metabolic emergency guidance.