What is the appropriate management for a patient presenting with hypoglycemia, leukocytosis, elevated hematocrit, metabolic alkalosis, and slightly elevated cardiac biomarkers, considering their good glucose control and slightly elevated estimated average glucose level?

Management of Laboratory Abnormalities in This Patient

Immediate Priority: Address the Artifactual Hypoglycemia

The reported glucose of 69 mg/dL is almost certainly a laboratory artifact caused by the marked leukocytosis (WBC 13.2, neutrophils 9.60), and does not represent true hypoglycemia requiring treatment. 1, 2, 3

Why This is Artifactual Hypoglycemia

• Leukocytosis causes in vitro glucose consumption by white blood cells between the time blood is drawn and when serum is separated for analysis, producing falsely low glucose readings even with WBC counts as low as 13,000-15,000/mm³ 1, 2, 3
• The patient is asymptomatic from a glucose perspective (no altered mental status, no confusion, no diaphoresis), which is the hallmark of artifactual rather than true hypoglycemia 1, 3
• The HbA1c of 5.9% and estimated average glucose of 123 mg/dL directly contradict true hypoglycemia and confirm normal-to-slightly elevated chronic glucose control 4
• True hypoglycemia at 69 mg/dL would produce symptoms including confusion, diaphoresis, tremor, and altered mental status—none of which are present 5

Confirm True Glucose Status

• Immediately recheck glucose using a point-of-care glucometer with fresh whole blood to obtain an accurate reading before any glucose administration 5
• If laboratory glucose measurement is required, request immediate centrifugation and separation of serum (within minutes of collection) or use a tube with glycolysis inhibitor (sodium fluoride) to prevent continued in vitro glucose consumption 2, 3
• Do not administer intravenous glucose based on the artifactual laboratory value, as this could cause iatrogenic hyperglycemia 5

---

Secondary Concern: Evaluate the Metabolic Alkalosis

The elevated CO2 of 36 mEq/L (bicarbonate) with normal anion gap (8) represents metabolic alkalosis, not diabetic ketoacidosis or other dangerous metabolic acidosis. 5

Rule Out DKA (Which This is NOT)

• This patient does NOT have DKA because: glucose is not >250 mg/dL (once corrected for artifact), bicarbonate is elevated not decreased, anion gap is normal not elevated, and pH would be alkalotic not acidotic 5, 6, 7
• DKA requires: glucose >250 mg/dL, pH <7.3, bicarbonate <15-18 mEq/L, and anion gap >10-12 mEq/L—none of which are present here 5, 6, 7

Determine Cause of Metabolic Alkalosis

• Check for volume depletion (elevated hematocrit 48.9% suggests hemoconcentration), which can cause contraction alkalosis 5
• Obtain detailed history of vomiting or nasogastric suction, as gastric HCl loss is a common cause of metabolic alkalosis even in diabetic patients 8
• Review diuretic use, particularly thiazides or loop diuretics, which cause chloride depletion and metabolic alkalosis 5
• Assess for mineralocorticoid excess if other causes are excluded 5

Management of Metabolic Alkalosis

• Administer isotonic saline (0.9% NaCl) if volume depletion is present, which will correct contraction alkalosis 5
• Replace potassium (current level 4.4 is acceptable but monitor closely) as hypokalemia perpetuates metabolic alkalosis 5
• Replace chloride through saline administration, as chloride-responsive alkalosis is most common 5

---

Tertiary Concern: Investigate the Leukocytosis

The WBC of 13.2 with neutrophilia (72.7%, absolute 9.60) requires identification of the underlying cause. 5

Systematic Evaluation

• Obtain blood cultures (already ordered per labs) and urine culture to identify occult infection, as infection is a common precipitant of metabolic derangements 5
• Review for recent corticosteroid use, which causes both leukocytosis and can precipitate hyperglycemic states 5
• Assess for acute stress response (trauma, surgery, myocardial infarction) given the slightly elevated troponin of 4 ng/L 5
• Consider inflammatory conditions if infectious and medication causes are excluded 5

Infection Workup

• Do not rely on temperature to rule out infection—patients can be normothermic or even hypothermic despite serious infection 5, 6, 7
• Procalcitonin of 0.03 is reassuringly low and argues against bacterial sepsis 5
• CRP of 0.4 is also low, making significant systemic inflammation less likely 5
• Complete the blood culture and add chest X-ray if any respiratory symptoms are present 5

---

Address the Elevated Hematocrit

The hematocrit of 48.9% likely represents hemoconcentration from volume depletion rather than true polycythemia. 5

Differentiate Hemoconcentration from Polycythemia

• Volume depletion is suggested by: elevated hematocrit, metabolic alkalosis, BUN/creatinine ratio of 28 (mildly elevated), and clinical context 5
• True polycythemia rubra vera would require: sustained elevation, elevated hemoglobin >16.5 g/dL in men or >16 g/dL in women, splenomegaly, and JAK2 mutation testing 1
• Current hemoglobin of 15.9 g/dL is at the upper limit of normal but not definitively elevated 1

Management

• Administer isotonic saline to correct volume depletion and reassess hematocrit after rehydration 5
• Recheck complete blood count after fluid resuscitation to determine if hematocrit normalizes 5
• If hematocrit remains elevated after adequate hydration, pursue polycythemia workup including JAK2 mutation, erythropoietin level, and hematology consultation 1

---

Evaluate the Cardiac Biomarkers

The troponin I of 4 ng/L is minimally elevated and requires correlation with clinical presentation and ECG findings. 5

Risk Stratification

• BNP of 41.0 pg/mL is normal (<100 pg/mL), making acute heart failure unlikely 5
• Obtain 12-lead ECG to assess for ST-segment changes, T-wave inversions, or other ischemic patterns 5
• Assess for chest pain, dyspnea, or other cardiac symptoms to determine if this represents acute coronary syndrome versus chronic troponin elevation 5

Management Based on Clinical Context

• If chest pain or ECG changes present: treat as acute coronary syndrome with aspirin, antiplatelet therapy, and cardiology consultation 5
• If asymptomatic with normal ECG: troponin elevation may be chronic (renal dysfunction, chronic heart disease) and requires outpatient cardiology follow-up 5
• Avoid aggressive glucose lowering (target 140-180 mg/dL if hyperglycemia confirmed) in the setting of potential cardiac ischemia to prevent hypoglycemia-induced ischemia 5

---

Critical Pitfalls to Avoid

• Never treat the artifactual glucose of 69 mg/dL with intravenous dextrose without first confirming true hypoglycemia with point-of-care testing 5, 1, 2, 3
• Never assume this is DKA based on diabetes history alone—the laboratory values definitively exclude DKA 5, 6, 7
• Never ignore infection as a precipitant even with normal temperature, as hypothermia or normothermia can occur with serious infection 5, 6, 7
• Never target tight glucose control (<150 mg/dL) in the setting of potential cardiac ischemia, as hypoglycemia can worsen ischemia 5