Supportive Care and Monitoring in Adrenal Insufficiency–Related Shock
Lesson Objective
Recommend appropriate supportive care and monitoring to manage complications associated with adrenal insufficiency–related shock.
1. Hemodynamic Support Measures
Relative adrenal insufficiency leads to profound vascular hyporesponsiveness to endogenous catecholamines and significant intravascular volume depletion. The cornerstone of management is rapid fluid resuscitation, followed by the prompt initiation of targeted vasopressors and stress-dose corticosteroids to restore tissue perfusion.
Case Vignette
An 80-year-old man with pneumonia presents with persistent hypotension (MAP < 60 mm Hg) despite receiving 3 L of normal saline. He is started on a norepinephrine infusion at 0.1 µg/kg/min. His MAP remains low until vasopressin 0.03 units/min is added as a second agent. Following this, the norepinephrine is weaned to 0.05 µg/kg/min. A hydrocortisone 100 mg IV bolus, followed by a 200 mg/day continuous infusion, is administered, achieving a stable MAP ≥ 65 mm Hg within 4 hours.
Vasopressor and Corticosteroid Selection
The primary indication for these therapies is fluid-refractory hypotension, defined as a mean arterial pressure (MAP) below 65 mm Hg after an initial crystalloid bolus of 30 mL/kg.
| Agent | Dosing | Key Monitoring | Pearls & Pitfalls |
|---|---|---|---|
| Norepinephrine | 0.01–3 µg/kg/min | Arterial waveform, ECG, lactate, urine output | Advantage: Potent vasoconstriction with minimal tachycardia. Pitfall: Risk of digital/mesenteric ischemia at high doses. |
| Vasopressin | 0.03 units/min (adjunct) | MAP response, signs of ischemia | Pearl: Spares catecholamines, stable heart rate. Warning: Avoid >0.06 units/min to reduce ischemic risk. |
| Epinephrine | 0.01–0.3 µg/kg/min | Heart rate, ECG, lactate, splanchnic perfusion | Use: Typically reserved for refractory hypotension after norepinephrine and vasopressin have been optimized. |
| Hydrocortisone | 100 mg IV bolus, then 50 mg IV q6h or 200 mg/day infusion | MAP response, blood glucose, electrolytes | Pearl: Initiate promptly; do not await ACTH stimulation test results in patients with shock. |
Key Pearls
- Early addition of vasopressin (e.g., when norepinephrine dose exceeds 0.25 µg/kg/min) can limit catecholamine toxicity and tachyphylaxis.
- Stress-dose hydrocortisone is critical for improving vasopressor responsiveness and accelerating shock reversal.
Editor’s Note on Mineralocorticoid Replacement
While stress-dose hydrocortisone provides sufficient mineralocorticoid activity for most patients in shock, some guidelines recommend adding fludrocortisone once the patient is hemodynamically stable and can tolerate oral medications. This is particularly relevant for patients with confirmed primary adrenal insufficiency. A complete protocol would include specific indications, dosing (e.g., 50 mcg PO daily), and electrolyte monitoring.
2. Prevention of ICU-Related Complications
The use of stress-dose steroids, while life-saving, can exacerbate common ICU complications by causing hyperglycemia, impairing mucosal defenses, and suppressing the immune system. Proactive, evidence-based protocols are essential to reduce morbidity.
Hyperglycemia Management
- Target Blood Glucose: Maintain a range of 140–180 mg/dL.
- Method: Use an algorithmic continuous insulin infusion (e.g., Yale protocol) with point-of-care glucose checks every 1–2 hours.
- Pitfall: Avoid relying on sliding-scale insulin alone, as it is associated with increased glycemic variability and poor control.
Stress Ulcer Prophylaxis (SUP)
- Agents: Proton pump inhibitors (PPIs) like Pantoprazole 40 mg IV daily, or H₂-receptor antagonists (H₂RAs) like Famotidine 20 mg IV every 12 hours.
- Indications: High-risk patients, including those on mechanical ventilation for >48 hours, those with coagulopathy, or those receiving high-dose steroids.
- Monitoring: Watch for signs of gastrointestinal bleeding and consider testing for Clostridioides difficile if diarrhea develops.
Infection Surveillance & Prophylaxis
- Strict adherence to Ventilator-Associated Pneumonia (VAP) and Central Line-Associated Bloodstream Infection (CLABSI) prevention bundles.
- Daily evaluation of all invasive lines and devices for necessity and signs of infection.
- Practice antimicrobial stewardship by de-escalating antibiotics when appropriate. Consider antifungal prophylaxis only in select, very high-risk patients.
Key Pearls
- Maintaining moderate glycemic control (140-180 mg/dL) is proven to reduce infection rates and improve outcomes in critically ill patients.
- De-escalate stress ulcer prophylaxis as soon as risk factors resolve to minimize the risk of hospital-acquired pneumonia and C. difficile infection.
3. Management of Corticosteroid Adverse Effects
Prolonged use of high-dose steroids carries significant risks, including metabolic derangements, opportunistic infections, myopathy, and gastrointestinal bleeding. A strategy focused on dose minimization and vigilant supportive care is required to mitigate these effects.
Hyperglycemia
Continue the insulin infusion as needed, maintaining moderate blood glucose targets. Monitor closely for hypoglycemia, especially as the steroid dose is tapered and the patient’s inflammatory state resolves.
Infection
Avoid routine systemic antibiotic prophylaxis. Instead, tailor infection prevention strategies to individual patient risks. Ensure vaccinations (e.g., influenza, pneumococcal) are updated once the patient is stable and approaching discharge. Daily sedation interruptions and early mobilization are key strategies to lower VAP risk.
Myopathy & GI Bleeding
The primary mitigation strategy is to employ the lowest effective glucocorticoid dose for the shortest possible duration. Initiate a rapid taper as soon as the patient is hemodynamically stable off vasopressors. Continue stress ulcer prophylaxis while the patient remains at high risk, and assess muscle strength and mobility daily to screen for critical illness myopathy.
Key Pearls
- Clinically significant steroid-induced myopathy typically manifests after 1–2 weeks of high-dose therapy and can delay liberation from mechanical ventilation.
- If the risk for C. difficile is high, a short-term course of a PPI is preferred for SUP. An H₂RA may be a suitable alternative for lower-risk patients to potentially reduce this risk.
4. Multidisciplinary Goals-of-Care Discussions
The decision to continue or taper prolonged corticosteroid therapy in critical illness is complex. It requires early, structured communication among the care team, patient, and family to align interventions with patient-centered goals and minimize iatrogenic harm.
Team Composition
Effective discussions should involve a multidisciplinary team, including critical care physicians, clinical pharmacists, palliative care specialists, bedside nursing staff, and rehabilitation therapists.
Discussion Focus
- Clearly outline the expected benefits versus the ongoing risks of steroid therapy.
- Establish a clear taper plan with defined monitoring checkpoints and criteria for pausing or restarting therapy.
- Provide comprehensive patient and family education on discharge, including instructions for emergency steroid injection techniques and the importance of medical alert identification.
Key Pearls
- Implementing standardized order sets with built-in steroid taper schedules and monitoring checklists can significantly reduce dosing errors and improve patient safety.
- Early documentation of goals of care and advance directives is crucial to ensure that all interventions, including steroid therapy, remain aligned with the patient’s wishes.
References
- Bornstein SR, Allolio B, Arlt W, et al. Diagnosis and Treatment of Primary Adrenal Insufficiency: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab. 2016;101(2):364–389.
- Kromah F, Tyroch A, McLean S, et al. Relative Adrenal Insufficiency in the Critical Care Setting: Debunking the Classic Myth. World J Surg. 2011;35(8):1818–1823.
- Marik PE, Pastores SM, Annane D, et al. Diagnosis and management of corticosteroid insufficiency in critically ill patients: consensus statements from an international task force. Crit Care Med. 2008;36(6):1937–1949.
