12-phase flow (10)

1. 1FRAME
   Glucocorticoid-induced HTN crisis = high-dose exogenous steroid (prednisone >20 mg/d, methylprednisolone, hydrocortisone) → mineralocorticoid receptor activation + Na+/water retention + K+ wasting + RAAS upregulation + vascular sensitization → severe HTN often with hypoK. Pharmacology pivot: IV nicardipine first-line for BP control + SPIRONOLACTONE 25-100 mg PO (or eplerenone if gynecomastia concern) to block the OFFENDING mineralocorticoid effect at the receptor + aggressive K/Mg replacement + reduce/convert steroid (switch to dexamethasone — minimal MR activity — when clinically possible) + treat the underlying disease with steroid-sparing alternatives. Route to parent engine for shared HTN-emergency arc; this dossier owns the steroid-specific pharmacology + cumulative-toxicity surveillance + steroid-sparing transition.
   inputs: sbp, dbp, heart_rate, glucocorticoid_med_history_and_indication, potassium
   advance: glucocorticoid-induced etiology confirmed (med history + dose + duration + hypoK pattern)
2. 2ENTRY
   Recognize cushingoid features + HTN + hypoK pattern; ECG within 10 min if chest pain or arrhythmia from hypoK; IV access × 2; cardiac monitor; initiate IV nicardipine + spironolactone PO
   inputs: age, sbp, glucocorticoid_med_history_and_indication
   advance: IV access + monitor + nicardipine started + spironolactone PO loading dose given
3. 3CONTEXT
   Glucocorticoid medication details (drug name, dose, route, duration, indication, taper status, prescriber); concurrent BP offenders (NSAIDs, sympathomimetics, OCPs, VEGF inhibitors, calcineurin inhibitors, MR-sparing diuretics); comorbidities (DM2 — HHS overlap risk; CKD — Na+ retention amplification; HF — preload sensitivity; immunosuppressed — opportunistic infection); endogenous-Cushing rule-out if no exogenous source apparent (24-h urine cortisol, dexamethasone suppression test, ACTH); psychiatric history (steroid psychosis); medication-adherence history
   inputs: age, concurrent_NSAID_or_other_BP_offenders
   advance: comprehensive med rec + steroid drug/dose/duration documented + concurrent offenders identified
4. 4RED_FLAGS
   Hypertensive encephalopathy (severe HA + AMS + papilledema); ICH (focal deficit + headache); aortic dissection (back pain + BP differential); HHS overlap from steroid-induced hyperglycemia (glucose >600 + osmotic symptoms); opportunistic infection on chronic steroid (PCP, aspergillosis, CMV reactivation, atypical mycobacterial); adrenal insufficiency on rapid taper (hypotension paradox + abdominal pain + AMS); steroid psychosis with suicide risk (dose-dependent — high-dose pulse methylprednisolone classic); severe hypoK <3.0 with arrhythmia; HF decompensation from Na+/water retention
   inputs: sbp, potassium, glucose, neurologic_exam
   actions: htn_emergency
   advance: RED flags screened + life-threats addressed + opportunistic infection + adrenal insufficiency + psychosis screen done
5. 5INITIAL_WORKUP
   BMP + Mg + Phos + glucose + troponin + CBC; ECG (LVH, arrhythmia from hypoK, demand ischemia); CXR (volume overload, opportunistic infection); urine K + plasma renin + aldosterone (TTKG / renin–aldo ratio for diff dx vs primary aldosteronism — both look similar but treatment overlaps anyway); 24-h urine cortisol or 1-mg dex suppression if endogenous Cushing suspected; HbA1c (steroid-DM screening); CT head non-con if neuro deficit; CTA chest if dissection concern; TTE if HF concern; infection workup if febrile or immunosuppressed (blood cultures, BAL if CXR infiltrate, CMV PCR if transplant)
   inputs: potassium, magnesium, creatinine, glucose, ecg_12_lead, troponin
   actions: panel.cardiac, panel.renal, panel.coag
   advance: workup documented + electrolytes corrected + ICH/dissection/MI/HHS/opportunistic infection ruled in/out
6. 6BRANCHING_WORKUP
   If ICH → AHA/ASA 2022 ICH pathway + IV nicardipine target SBP 130-140; if dissection → CTA + emergency CT surgery + parent aortic-dissection HTN engine; if MI → cardiology + ACS pathway; if HHS → endo HHS protocol + insulin drip + IV fluids + electrolyte correction (concurrent steroid HTN management); if PCP/opportunistic infection → ID + treat infection + reduce steroid; if adrenal insufficiency from over-rapid taper → STRESS-DOSE HYDROCORTISONE 100 mg IV bolus then 50-100 mg IV q6-8h + slow re-taper; if endogenous Cushing diagnosed → endocrine surgery referral
   advance: syndrome-specific pathway activated if needed
7. 7TREATMENT
   STEP 1 — IV NICARDIPINE 5-15 mg/h titrate to MAP-↓ ≤25% in first hour, SBP <160 within 2 h (parent HTN-emergency target). STEP 2 — SPIRONOLACTONE 25-100 mg PO (block the offending MR effect; titrate per K + BP); eplerenone 25-50 mg PO BID alternative if gynecomastia concern; loading 50-100 mg PO once for severe. STEP 3 — Aggressive K + Mg replacement (KCl 40-60 mEq IV/PO + MgSO4 2-4 g IV; target K 4-5, Mg 2). STEP 4 — Steroid review with prescriber: REDUCE DOSE if clinically possible OR CONVERT to lower-MR-activity agent (switch to dexamethasone 0.75 mg = 5 mg prednisone equivalent, minimal MR activity). STEP 5 — Add IV labetalol 10-20 mg q10 min if persistent HTN despite nicardipine + spironolactone. STEP 6 — Add loop diuretic (furosemide 20-40 mg IV) if volume overload (cautious — avoid worsening hypoK; use only with K replacement + spironolactone protection). STEP 7 — Treat underlying disease with steroid-sparing alternative if appropriate (DMARDs, biologics, calcineurin inhibitor). AVOID: simply stopping steroid abruptly (adrenal insufficiency risk if chronic >2 weeks use — taper); avoid simultaneous NSAID continuation (synergistic toxicity).
   inputs: sbp, dbp, potassium, magnesium
   advance: BP at target SBP <160 + spironolactone started + K/Mg corrected + steroid review/reduction documented
8. 8DISPOSITION
   ICU / step-down for q15 min BP + telemetry minimum 24 h; HHS + opportunistic infection + adrenal insufficiency surveillance; rheumatology / ID / endocrinology / oncology consult per underlying disease; pharmacy + outpatient steroid-sparing planning
   advance: monitored bed assigned + 24-h observation plan + multidisciplinary consults requested
9. 9MONITORING
   Continuous ECG + telemetry; q15-30 min BP; q4-6h BMP + Mg until normalized; daily glucose checks (steroid-DM); daily weight (volume status); serial neuro exam q2h × 12 h; UOP; infection surveillance (temp, WBC, CXR if respiratory symptoms)
   inputs: sbp, potassium, glucose
   actions: panel.cardiac, panel.coag
   advance: BP at target + electrolytes normal + no organ damage + steroid-sparing plan in place
10. 10FOLLOWUP
    STEROID MINIMIZATION: confirmed plan to taper to lowest effective dose (or off) over 4-12 weeks per indication + disease control; STEROID-SPARING TRANSITION: rheum/ID/onc-led DMARD/biologic/calcineurin-inhibitor introduction with overlap (MTX, hydroxychloroquine, azathioprine, cyclosporine, biologics like rituximab/tocilizumab/TNFi); PROPHYLACTIC SPIRONOLACTONE 25-50 mg PO daily during ongoing high-dose courses; BP MONITORING: weekly home BP during steroid taper, monthly during chronic low-dose maintenance; K MONITORING: q1-2 weeks during steroid + spironolactone titration; STEROID-RELATED COMPLICATION SURVEILLANCE: bone density (DEXA + bisphosphonate prophylaxis if >5 mg prednisone equivalent for ≥3 months — ACR 2017 PMID 28585410), HbA1c (steroid-DM screening q3 months), lipid panel, ophthalmology (cataracts, glaucoma), PCP prophylaxis if >20 mg prednisone for ≥1 month (TMP-SMX or atovaquone), VZV reactivation surveillance, vaccination optimization (avoid live vaccines on >20 mg prednisone); ADRENAL AXIS RECOVERY: stress-dose protocol issued + medical-alert bracelet for chronic steroid users; PSYCHIATRIC follow-up if steroid psychosis history; PCP + endocrinology + relevant specialty (rheum/ID/onc) follow-up within 1-2 weeks
    advance: steroid taper plan documented + steroid-sparing transition initiated + prophylactic spironolactone + bone protection + glucose monitoring + adrenal recovery plan + 1-2 wk follow-up booked