DKA and HHS

Diabetes Basics

Diagnosis of Diabetes

• A1C: ≥6.5%

• FPG: ≥126 mg/dL (after ≥8 hrs fasting)

• 2-hr OGTT: ≥200 mg/dL (after 75 g glucose load)

• Random glucose: ≥200 mg/dL with symptoms (3 P’s: polyuria, polydipsia, polyphagia).

Diabetic Ketoacidosis (DKA)

Epidemiology

• More common in Type 1 DM.

• Can occur in Type 2 during severe stress/illness.

Causes (6 I’s)

1. Insulin (lack or noncompliance, undiagnosed DM).

2. Infection.

3. Inflammation (pancreatitis).

4. Intoxication (drugs/alcohol).

5. Infarction (MI, stroke).

6. Iatrogenic (glucocorticoids, stress).

Pathophysiology

• Absolute insulin deficiency → glucose cannot enter cells.

• Body breaks down fat → ketones → metabolic acidosis.

• Osmotic diuresis → dehydration, electrolyte loss.

Clinical Manifestations

• Lethargy, weakness (early).

• Dehydration signs: dry mucous membranes, poor turgor, tachycardia, orthostatic hypotension.

• GI: anorexia, N/V, abdominal pain.

• Respiratory: Kussmaul respirations (deep, rapid).

• Fruity breath odor (acetone).

Diagnostic Criteria

• Blood glucose ≥250 mg/dL.

• pH <7.30.

• Bicarbonate <16 mEq/L.

• Moderate to high ketones (urine or serum).

Anion Gap (“closing the gap”)

• Formula: (Na + K) – (Cl + HCO₃).

• Normal: 3–11.

Treatment (Stepwise)

1. Airway + Oxygen.

2. IV access & fluids:

   • Start with 0.9% or 0.45% NS, 1 L/hr.

   • Add D5 with NS when BG <250 to prevent hypoglycemia/cerebral edema.

3. Regular insulin IV drip 0.1 U/kg/hr (drop BG by 36–54 mg/dL/hr).

4. Potassium replacement: even if normal initially, insulin & fluids drive K⁺ into cells → hypokalemia risk.

5. Bicarb replacement only if severe acidosis (pH <7.0).

Nursing Priorities

• Monitor: vitals, LOC, ECG, O₂ sat, urine output.

• Assess breath sounds (fluid overload).

• Labs: glucose, K⁺, bicarb.

• Prevent hypoglycemia and cerebral edema with careful titration.

• Patient teaching: insulin adherence, sick-day rules, early recognition of symptoms.

Hyperosmolar Hyperglycemia Syndrome (HHS)

Epidemiology

• More common in Type 2 DM, usually in older adults (>60).

• Often with comorbidities (infection, illness, dehydration, poor fluid intake).

Pathophysiology

• Some insulin present → no ketones/acidosis.

• Severe hyperglycemia → osmotic diuresis → dehydration & hyperosmolarity.

• Neurological manifestations due to cellular dehydration (confusion, seizures, coma).

Clinical Manifestations

• Very high BG: >600 mg/dL.

• Dry mouth, extreme thirst, polyuria.

• Warm, dry skin, fever >101°F.

• Hypotension, tachycardia.

• Neuro: somnolence, confusion, hallucinations, hemiparesis, seizures, vision loss.

Labs

• BG >600 mg/dL.

• Osmolality ↑.

• Little/no ketones.

Treatment

1. Fluids: 0.9% or 0.45% NS; 1st hr 10–30 mL/kg, then 500–1000 mL/hr.

2. IV insulin drip (regular insulin). Transition to SQ when stable.

3. Add D5 fluids when BG 250–300.

4. Electrolyte correction: monitor K⁺, Na⁺, Mg²⁺, phosphate.

5. Slow normalization of glucose (50–100 mg/dL/hr) to prevent cerebral edema.

Nursing Priorities

• Frequent BG & electrolyte checks (q1–2 hrs).

• Strict I&O.

• Monitor VS, mental status, ECG.

• Maintain safety (HOB ↑, aspiration precautions).

• Watch for complications: hypoglycemia, ARDS, dysrhythmias, sepsis, cerebral edema.

Key Differences: DKA vs HHS

NCLEX Quick Review

• DKA hallmark: Kussmaul respirations + fruity breath.

• HHS hallmark: Extreme hyperglycemia + neuro symptoms, no acidosis.

• DKA priority: Fluids first, then insulin.

• Add dextrose fluids when BG <250 (DKA) or <300 (HHS).

• Monitor K⁺ closely in both.

• Sick-day rules: Never stop insulin, hydrate, check BG/ketones frequently.