Supportive Care and Complication Management in Hyperglycemic Crises (DKA & HHS)

1. Organ Support Measures

Severe metabolic derangements in DKA/HHS may precipitate respiratory failure or hemodynamic collapse. Prompt recognition and targeted support maintain perfusion and oxygenation while metabolic therapy proceeds.

A. Respiratory Support

• Indications for mechanical ventilation:
  • Glasgow Coma Scale ≤8 or inability to protect airway
  • Refractory hypoxemia (PaO₂/FiO₂ <200) despite oxygen
  • Hypercapnia with pH <7.20 or respiratory muscle fatigue
• Ventilator strategies:
  • Lung-protective settings: tidal volume 6 mL/kg predicted body weight; plateau pressure <30 cm H₂O; PEEP to recruit alveoli
  • Adjust minute ventilation to target pH 7.25–7.35; avoid excessive hyperventilation once metabolic acidosis resolves
  • Monitor arterial blood gases every 2–4 hours during the acute phase

B. Hemodynamic Support

• Persistent hypotension (MAP <65 mmHg) after 30–60 mL/kg isotonic crystalloid indicates need for vasopressors.
• First-line agent: norepinephrine 0.05–0.1 µg/kg/min, titrated to MAP ≥65 mmHg.
• Adjunct: vasopressin 0.03 units/min to reduce catecholamine dose and support renal perfusion.
• Monitoring:
  • Invasive arterial line for continuous pressure monitoring.
  • Lactate clearance and urine output >0.5 mL/kg/h as perfusion surrogates.
  • Echocardiographic assessment (e.g., stroke volume variation) in patients with cardiac comorbidity.

2. ICU-Related Prophylaxis

Hyperglycemic crises create prothrombotic, stress-ulcer, and infection risks. Standard ICU prophylaxis mitigates these complications and supports recovery.

A. Venous Thromboembolism (VTE) Prophylaxis

• Agent: enoxaparin 40 mg SC once daily (if CrCl <30 mL/min: 30 mg SC once daily).
• Consider Anti-Xa monitoring (target 0.2–0.5 IU/mL) in extremes of weight or severe renal dysfunction.
• Contraindications: platelet count <50×10³/µL. Use intermittent pneumatic compression devices until platelets recover.

B. Stress Ulcer Prophylaxis

• Options: Proton pump inhibitor (PPI) like pantoprazole 40 mg IV daily, or an H2-receptor antagonist (H2RA) like ranitidine 50 mg IV every 8 hours.
• PPI Pros/Cons: Potent, prolonged acid suppression versus a potential increased risk of hospital-acquired pneumonia and C. difficile infection.
• De-escalation: Discontinue prophylaxis when full enteral nutrition is established (typically within 48–72 hours).

C. Infection Prevention

• Glycemic Target: Maintain blood glucose between 140–180 mg/dL using a validated insulin-infusion protocol; monitor glucose every 1–2 hours.
• Central‐line Bundles: Adhere strictly to maximal barrier precautions, chlorhexidine skin prep, and daily review of line necessity.
• Device Management: Remove unnecessary catheters and lines promptly to reduce the risk of device-associated infections.

3. Management of Iatrogenic Complications

Aggressive metabolic therapy can cause hypoglycemia, hypokalemia, fluid overload, and—rarely—cerebral edema. Vigilant monitoring and timely interventions prevent morbidity and mortality.

A. Hypoglycemia

• Definition: Blood glucose <70 mg/dL (action threshold often <54 mg/dL).
• Treatment:
  • Symptomatic or <70 mg/dL: 25 g IV dextrose (one ampule of D50W).
  • Asymptomatic <54 mg/dL: 10 g IV dextrose (e.g., 100 mL of D10W).
• Infusion adjustments: Reduce insulin rate by 50% or temporarily hold until glucose is >100 mg/dL.

B. Hypokalemia

• Risk: Intracellular shift of potassium driven by insulin therapy, compounded by urinary losses from osmotic diuresis and dilution from volume resuscitation.
• Monitoring: Serum potassium every 2–4 hours during the acute phase.
• Replacement: Add 20–40 mEq KCl to each liter of IV fluid to maintain serum levels. Infusion rates should not exceed 20 mEq/h via peripheral line or 40 mEq/h via central line (with continuous telemetry).
• Insulin delay: If initial serum K+ is <3.3 mEq/L, hold insulin and replete potassium first.

C. Fluid Overload

• Recognition: New pulmonary crackles, jugular venous distension, positive fluid balance >2 L/24 h, or new/worsening peripheral edema.
• Management:
  • Reduce maintenance fluid rate to 1.5–2 mL/kg/h.
  • Administer a loop diuretic (e.g., furosemide 20–40 mg IV) and titrate based on urine output.
  • Monitor daily weights, strict intake/output, and chest imaging as needed.

D. Cerebral Edema

• Early warning signs: Headache, bradycardia, hypertension (Cushing’s triad), or altered mental status despite metabolic improvement.
• Immediate therapy:
  • Mannitol 0.5–1 g/kg IV over 20 minutes OR Hypertonic saline (3%) 5–10 mL/kg over 30 minutes.
  • Elevate head of bed to 30 degrees.
  • If intubated, provide controlled ventilation to a target PaCO₂ of 30–35 mmHg.
  • Reduce fluid infusion rate by 50% and obtain emergent neuroimaging (CT head).

4. Multidisciplinary Goals-of-Care Discussions

In refractory or complicated hyperglycemic crises, multidisciplinary and ethical frameworks guide invasive support decisions while honoring patient values.

A. Ethical Framework

Discussions should be guided by core principles of medical ethics:

• Beneficence: Acting in the best interest of the patient.
• Non-maleficence: Avoiding harm.
• Autonomy: Respecting the patient’s right to make decisions about their own care.
• Proportionality: Ensuring the potential benefits of interventions outweigh the burdens.

B. Palliative Care and Family Engagement

• Consider early palliative care consultation for complex symptom management and to help clarify goals of care.
• Conduct regular interdisciplinary family meetings involving critical care, endocrinology, pharmacy, and nursing to ensure consistent communication.

C. Documentation and Shared Decision-Making

• Clearly document all discussions regarding risks, benefits, alternatives, and patient/family preferences.
• Ensure advance directives and code status are clearly recorded and accessible.
• Revisit goals of care as the clinical status evolves to ensure that ongoing treatment aligns with the patient’s expressed values.