6.1 Glycemic Emergencies

Diabetic Ketoacidosis (DKA)

Diabetic ketoacidosis (DKA) is an acute metabolic decompensation caused by an absolute or relative deficiency of insulin combined with a rise in counter-regulatory hormones (glucagon, catecholamines, cortisol, growth hormone). Without insulin, cells cannot use glucose, so the liver over-produces glucose and breaks down fat into free fatty acids that are converted to ketone bodies (beta-hydroxybutyrate and acetoacetate). These ketoacids drive a high anion gap metabolic acidosis. DKA is classically a complication of type 1 diabetes but can occur in type 2, and it is frequently precipitated by Infection, Insulin omission, Ischemia (MI), and Intoxication — the "4 I's" the CCRN loves to test.

Diagnostic thresholds

DKA is defined by the triad of hyperglycemia, ketosis, and acidosis:

• Glucose >250 mg/dL (usually 350-800, but can be lower in euglycemic DKA from SGLT2 inhibitors or pregnancy)
• Arterial pH <7.3 and serum bicarbonate <18 mEq/L
• Positive serum/urine ketones (beta-hydroxybutyrate is the more sensitive test)
• Elevated anion gap (Na − [Cl + HCO3]) >10-12 mEq/L

Severity is graded mild-to-severe by pH and mental status; severe DKA has pH <7.0 and stupor/coma. Kussmaul respirations (deep, rapid breathing) represent respiratory compensation for the acidosis, and a fruity acetone odor may be present.

Managing DKA: fluids, insulin, potassium

The order of interventions is critical and is the single most tested DKA concept. Memorize the sequence: fluids first, then insulin, with potassium managed continuously.

1. IV fluids first. Begin with isotonic 0.9% normal saline, often 15-20 mL/kg (about 1-1.5 L) in the first hour to restore intravascular volume. Volume alone lowers glucose and improves perfusion. Once corrected sodium and volume improve, switch to 0.45% saline.
2. Insulin infusion. Start a regular insulin infusion at roughly 0.1 unit/kg/hr (a bolus is optional and increasingly omitted). Insulin shuts off ketogenesis and closes the anion gap. The goal is to lower glucose by ~50-75 mg/dL per hour — faster drops risk cerebral edema.
3. Potassium replacement. Total-body potassium is always depleted even when the measured serum K+ looks normal or high, because acidosis shifts K+ out of cells. As insulin and fluids correct the acidosis, K+ moves back intracellularly and the serum level falls sharply.

The potassium safety rule

Before or during insulin therapy, check the potassium:

Giving insulin when K+ is <3.3 mEq/L drives the remaining potassium into cells and can cause life-threatening hypokalemia and arrhythmias — a classic CCRN trap.

Adding dextrose

When the glucose falls to approximately 200-250 mg/dL, add IV dextrose (D5) to the fluids. This is counterintuitive but essential: the anion gap and ketosis usually have NOT yet resolved, so the insulin infusion must continue to clear ketones. Dextrose lets you keep insulin running without causing hypoglycemia. The endpoints for DKA resolution are anion-gap closure and bicarbonate normalization, NOT simply a normal glucose. Do not stop the IV insulin abruptly; overlap with subcutaneous insulin for 1-2 hours to prevent rebound ketosis.

Cerebral edema risk

Cerebral edema is a feared, potentially fatal complication, most common in children and adolescents but tested for all ages. It is associated with overly rapid correction of glucose and osmolality and aggressive fluid administration. Signs include worsening headache, deteriorating mental status, bradycardia, and hypertension. Prevention is measured correction; treatment is mannitol or hypertonic saline and elevating the head of bed.

Hyperosmolar Hyperglycemic State (HHS)

HHS occurs typically in older type 2 diabetics with a precipitating illness. Enough endogenous insulin is present to suppress ketogenesis, so patients do NOT develop significant acidosis, but glucose climbs to extreme levels, driving an osmotic diuresis and profound dehydration. HHS is distinguished from DKA by glucose often >600 mg/dL, serum osmolality >320 mOsm/kg, minimal/absent ketosis, and pH >7.3. Neurologic changes (obtundation, seizures, coma) are prominent because of the marked hyperosmolality. Mortality is higher than DKA (up to 10-20%). Treatment mirrors DKA — the cornerstone is aggressive fluid resuscitation to correct the severe volume deficit (often 8-10 L), followed by a lower-rate insulin infusion and cautious potassium replacement.

Hypoglycemia

Hypoglycemia (glucose <70 mg/dL, severe <54 mg/dL) is an immediate threat to the brain. In the ICU it commonly complicates insulin infusions, sepsis, hepatic/adrenal failure, and tight glycemic control. Adrenergic signs (diaphoresis, tremor, tachycardia) give way to neuroglycopenic signs (confusion, seizures, coma). A patient on a DKA insulin infusion who becomes diaphoretic, tremulous, and confused with a glucose of 48 mg/dL needs the hypoglycemia treated first: give IV dextrose (D50) in the conscious/IV-access patient (or IM glucagon if no access), then recheck the glucose and adjust the infusion per protocol. Do not delay treatment to hunt for a cause.

Monitoring and common CCRN traps

During resuscitation, the CCRN nurse trends hourly point-of-care glucose, serial basic metabolic panels every 2-4 hours for the anion gap, potassium, and corrected sodium, and continuous ECG for hypo/hyperkalemic changes (peaked T waves, U waves). Watch for the refractory hypokalemia produced by coexisting hypomagnesemia: a chronic-alcohol patient with a magnesium of 1.0 mg/dL whose potassium will not rise despite replacement needs magnesium repleted first, because low magnesium promotes renal potassium wasting and blocks correction. Two additional traps recur on the exam. First, euglycemic DKA — driven by SGLT2 inhibitors, pregnancy, or starvation — presents with a near-normal glucose but a wide anion gap and ketosis; treat it as DKA with fluids, insulin, and early dextrose, not as a mild case. Second, the corrected sodium: hyperglycemia falsely lowers measured sodium (add ~1.6-2.0 mEq/L per 100 mg/dL of glucose above 100), so a "low" sodium may actually be normal or high, guiding your fluid choice. Finally, follow phosphate; severe hypophosphatemia during treatment can impair respiratory muscle strength and is replaced when the level drops below ~1.0 mg/dL.