← Back to dossier
Patient handout

Cushing syndrome HTN crisis (cortisol-excess–driven severe HTN with hypokalemic alkalosis)

PRODUCTION

1. Your condition

This handout is for cushing syndrome htn crisis (cortisol-excess–driven severe htn with hypokalemic alkalosis). Your care team identified this based on: cushingoid phenotype (moon facies, dorsocervical fat pad, central obesity, purple striae, proximal myopathy, easy bruising) + severe htn (newell-price lancet 2006 pmid 16713505).

Other reasons your team may use this plan: severe hypokalemia (k <3.0) + metabolic alkalosis + htn — high-cortisol or ectopic acth suspicion; chronic supraphysiologic glucocorticoid exposure (prednisone ≥7.5 mg ≥3 wk, dexamethasone, megestrol, intra-articular/inhaled high-dose) — exogenous cushing; pituitary microadenoma or adrenal incidentaloma + htn + hypokalemia → biochemical cushing screen.

2. Your medications

Take these medications exactly as prescribed. Do not stop or change a dose without talking to your provider.

MedicationStarting doseHowWhenWhat it does
nicardipine5 mg/h IV titrate by 2.5 mg/h q5-15 min, max 15 mg/hIVcontinuousACC/AHA 2025 — predictable titration; safe in Cushing with renal involvement; CCB preferred acute
spironolactone25-50 mg PO daily, titrate to 100-400 mg/dPOdailyEndocrine Society 2008/2015 (PMID 18334580/26222757) — blocks MR activation by cortisol; addresses K wasting + HTN simultaneously; gynecomastia limit (use eplerenone if concern)
eplerenone25-50 mg PO daily, titrate to 100-200 mg/dPOdaily or BIDSelective MR antagonist — no androgen receptor blockade → no gynecomastia; less potent than spironolactone, requires higher doses; PATHWAY-2 PMID 26414968 demonstrated MRA efficacy in resistant HTN
potassium chlorideKCl IV 10-20 mEq/h via central line if K <3 (peripheral max 10 mEq/h); KCl PO 40-80 mEq dividedIV + POcontinuous IV or QID POSevere hypokalemia from cortisol-driven K wasting; replace to ≥3.5 with continuous ECG monitoring
magnesium sulfate2-4 g IV load + 1-2 g/h infusionIVcontinuousMg almost always coexisting low; refractory hypokalemia without Mg correction; Torsades prophylaxis
ketoconazole200 mg PO TID, titrate to 400-1200 mg/d dividedPOTID-QIDEndocrine Society 2015 (PMID 26222757) — CYP17 + CYP11B inhibitor; rapid cortisol-lowering; HEPATOTOXICITY (monitor LFTs weekly initial then monthly); QT prolongation; CYP3A4 interactions
metyrapone250 mg PO QID, titrate to 500-1000 mg q6hPOQIDEndocrine Society 2015 — 11β-hydroxylase inhibitor; rapid effect; can cause hirsutism + hypoadrenalism; alternative when ketoconazole hepatic concern
osilodrostat2 mg PO BID, titrate q2 wk to max 30 mg BIDPOBIDLINC-3 trial (Fleseriu Lancet Diabetes Endocrinol 2019 PMID 31523029) — newer 11β-hydroxylase inhibitor + aldosterone synthase inhibitor; FDA approved Cushing disease 2020; hyperandrogenism + adrenal insufficiency monitor
mifepristone300 mg PO daily, titrate to 600-1200 mg/dPOdailyFDA approved (Korlym) for Cushing-induced hyperglycemia; SEEKING-2 trial; cortisol levels rise (GR antagonism not synthesis inhibition) — cannot use cortisol to titrate; symptom-based + glucose-based titration; HYPOKALEMIA worsens (need MRA + K)
mitotane0.5 g PO BID titrate to 4-8 g/d (target plasma 14-20 mg/L)POBID-TIDEndocrine Society 2015 — adrenolytic agent specific for adrenocortical carcinoma; slow onset (weeks); GI + neuro toxicity; mandatory cortisol replacement during therapy; long terminal half-life
AVOID isolated ACEi/ARB acutelyAVOIDN/AN/ACushing patients have aldosterone-like activity but renin-suppressed RAAS → ACEi alone less effective; coexisting hypokalemia + risk of hyperK if MRA also added → start MRA + K replacement first, then ACEi/ARB once K stable
STOP exogenous glucocorticoid (taper if iatrogenic)Taper (do not stop abruptly — adrenal suppression risk)PO/inhaled/topicaltaperIatrogenic Cushing from chronic supraphysiologic GC — taper with stress-dose coverage during illness; CRH-stim or AM cortisol to confirm HPA recovery before full stop

Plan: Cushing syndrome HTN crisis — MR-blockade FIRST (spironolactone or eplerenone) + K replacement + nicardipine; cortisol-lowering bridge (ketoconazole, metyrapone, osilodrostat, mifepristone, mitotane) for surgical bridge

3. When to call your provider

Contact your care team if any of the following happen:

  • Recurrent symptoms → urgent UFC + DST + imaging
  • Adrenal crisis intercurrent illness → IV hydrocortisone + ED
  • New cushingoid changes → re-eval for recurrence

4. When to seek emergency care

Call 911 or go to the nearest emergency room right away if you have:

  • Cushing patient with severe hypercortisolism (UFC >1000 mcg/24h or 4× ULN) develops fever, hypoxia, infiltrate — opportunistic infection (PJP, CMV, aspergillosis, candidemia) from cortisol immunosuppression(life-threatening)
  • Cushing crisis + glucose >600 mg/dL + osmolality >320 + altered mental status → hyperglycemic hyperosmolar state from cortisol-induced extreme insulin resistance(life-threatening)
  • Ectopic ACTH from SCLC, bronchial carcinoid, MTC, pheo — metastatic at presentation with severe Cushing crisis + hypokalemia <2.5 + cachexia(life-threatening)
  • Cushing patient with new psychosis, severe depression, mania, or suicidal ideation — psychiatric symptoms in 50-80% Cushing, suicide risk elevated
  • Cushing disease patient with known pituitary macroadenoma develops sudden severe headache + visual field defect + altered mental status + hypopituitarism — pituitary apoplexy (hemorrhagic infarct of adenoma)(life-threatening)

5. Follow-up

Postop morning cortisol day 1-3 (suppression to <1.8 mcg/dL = remission); if <5 — physiologic hydrocortisone replacement 15-25 mg/d divided BID (or 10/5 split); follow ACTH stim test annually until HPA recovery (usually 6-18 mo); annual UFC + ACTH for recurrence (10-15% recurrence at 10 years for Cushing disease); cardiovascular risk reassessment (cardiometabolic legacy effect persists years after cure); bone density DEXA + osteoporosis treatment; psychiatric follow-up (mood symptoms slow recovery); diabetes management (often resolves but chronic GI insulin resistance may persist)

6. Sources

Guideline: Endocrine Society 2008 Cushing Syndrome Diagnosis CPG (Nieman JCEM 2008 PMID 18334580) + 2015 Treatment CPG (Nieman JCEM 2015 PMID 26222757) + 2025 ACC/AHA HTN (Whelton)

  1. pubmed.ncbi.nlm.nih.gov/18334580
  2. pubmed.ncbi.nlm.nih.gov/26222757
  3. pubmed.ncbi.nlm.nih.gov/26142020