12-phase flow (10)

1. 1FRAME
   NSAID-induced HTN crisis = COX inhibition → reduced prostaglandin → loss of renal afferent vasodilation + reduced natriuresis + RAAS upregulation + Na+/water retention + endothelial vasoconstriction → severe HTN. Most vulnerable: CKD, HF, elderly, cirrhosis, on ACEi/ARB/diuretic ("triple whammy" → AKI). Pharmacology pivot: STOP NSAID immediately + IV nicardipine first-line for BP control + FUROSEMIDE 20-40 mg IV (overcomes renal Na+ retention from prostaglandin loss) + spironolactone if hypoK + IV labetalol adjunct. Long-term: AVOID NSAIDs in vulnerable patients; substitute acetaminophen (1 g q6h max 3-4 g/d), topical NSAID (minimal systemic), duloxetine for chronic musculoskeletal, opioid for severe with caution, gabapentinoid for neuropathic, intra-articular steroid for joint-specific. Route to parent engine for shared HTN-emergency arc; this dossier owns NSAID-specific pharmacology + triple-whammy AKI prevention.
   inputs: sbp, dbp, heart_rate, NSAID_med_history_dose_duration_indication, creatinine
   advance: NSAID-induced etiology confirmed (med history + dose + duration + electrolyte/renal pattern)
2. 2ENTRY
   Recognize triple-whammy (NSAID + ACEi/ARB + diuretic) or chronic NSAID exposure with HTN; ECG within 10 min if chest pain; IV access × 2; cardiac monitor; STOP NSAID immediately; initiate IV nicardipine + furosemide IV
   inputs: age, sbp, NSAID_med_history_dose_duration_indication
   advance: IV access + monitor + NSAID stopped + nicardipine started + furosemide given
3. 3CONTEXT
   NSAID medication details (drug name, dose, route, duration, indication, OTC vs prescription source, frequency); concurrent BP/AKI offenders (ACEi/ARB, diuretic — triple whammy; SGLT2i; aminoglycosides; iodinated contrast; PPI); comorbidities (CKD — KDIGO stage matters; HF — preload sensitivity; cirrhosis — splanchnic vasodilation reverses; elderly — frailty + polypharmacy; volume depletion); pain etiology (need for ongoing analgesia — what alternative?); allergies; surgery history (post-op ketorolac scenario)
   inputs: age, concurrent_ACEi_ARB_diuretic_RAAS_blocker
   advance: comprehensive med rec + NSAID drug/dose/duration + concurrent triple-whammy components identified + pain etiology characterized for alternative planning
4. 4RED_FLAGS
   Hypertensive encephalopathy (severe HA + AMS + papilledema); ICH (focal deficit + headache); aortic dissection (back pain + BP differential); triple-whammy AKI requiring dialysis (oliguria + Cr doubling + uremia); GI bleed on NSAID + anticoagulant or antiplatelet (hematemesis, melena, dropping Hb — high mortality combination); recurrent NSAID exposure error (system failure suggests adherence/awareness gap); CV event on selective COX-2 (rofecoxib withdrawal + celecoxib class signal — Solomon Circulation 2008 PMID 18506014); HF decompensation from Na+/water retention + RAAS dysregulation; severe hyperK from NSAID + ACEi combination
   inputs: sbp, creatinine, potassium, neurologic_exam
   actions: htn_emergency
   advance: RED flags screened + life-threats addressed + AKI staged + GI bleed screen + CV event rule-out done
5. 5INITIAL_WORKUP
   BMP + Mg + Phos + glucose + troponin + CBC + coags + LFTs (NSAID hepatotoxicity); urine analysis + urine sodium + FENa for AKI characterization (prerenal vs intrinsic); ECG (LVH, arrhythmia, demand ischemia); CXR (volume overload from Na+ retention); type and screen if GI bleed concern; CT head non-con if neuro deficit; CTA chest if dissection concern; TTE if HF concern; renal ultrasound if AKI to exclude obstruction; CT abdomen if peritonitis concern from perforated NSAID ulcer
   inputs: creatinine, potassium, sodium, magnesium, ecg_12_lead, troponin
   actions: panel.cardiac, panel.renal, panel.coag
   advance: workup documented + AKI staged + electrolytes assessed + ICH/dissection/MI/GI bleed/perforation 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 AKI requiring dialysis → nephrology emergent + CRRT/HD initiation; if GI bleed on NSAID + anticoagulant → GI emergent + endoscopy + reversal of anticoagulant; if CV event on selective COX-2 → cardiology + reassess COX-2 use; if perforated ulcer → general surgery emergent
   advance: syndrome-specific pathway activated if needed
7. 7TREATMENT
   STEP 1 — STOP NSAID IMMEDIATELY (any route — PO, IV, topical absorption can also contribute though minor). STEP 2 — IV NICARDIPINE 5-15 mg/h titrate to MAP-↓ ≤25% in first hour, SBP <160 within 2 h (parent HTN-emergency target). STEP 3 — FUROSEMIDE 20-40 mg IV (overcomes renal Na+ retention from prostaglandin loss; standard loop diuretic for volume overload + RAAS dysregulation in NSAID HTN). STEP 4 — Spironolactone 25-50 mg PO if hypoK from concurrent loop diuretic, OR DISCONTINUE spironolactone if hyperK from triple whammy. STEP 5 — Hold ACEi/ARB acutely if AKI / hyperK (avoid worsening — can resume once renal function stabilizes); if not in AKI, can continue with monitoring. STEP 6 — IV labetalol 10-20 mg q10 min adjunct if persistent HTN. STEP 7 — IV fluids (NS 250-500 mL bolus) if prerenal AKI from over-diuresis or volume depletion (cautious if HF). STEP 8 — Pain control with ALTERNATIVE: acetaminophen 1 g IV/PO q6h (max 3-4 g/d), topical lidocaine, intra-articular steroid for joint-specific pain, opioid for severe acute pain (caution — multimodal), gabapentinoid for neuropathic. STEP 9 — Dialysis if severe AKI with uremia, hyperK, acidosis, or volume overload refractory to diuresis (KDIGO 2024 AKI). AVOID: continuing NSAID for any reason, restarting NSAID without reason for vulnerability resolved.
   inputs: sbp, dbp, creatinine, potassium
   advance: NSAID stopped + BP at target + AKI managed + alternative pain control plan started
8. 8DISPOSITION
   ICU / step-down for q15 min BP + telemetry minimum 24 h; AKI surveillance + nephrology consult; pain medicine consult for chronic pain alternative regimen; GI consult if bleed concern
   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 creatinine + UOP for AKI tracking; daily weight (volume status); serial neuro exam q2h × 12 h; pain scale assessment with alternative regimen; GI bleed surveillance (Hb, BUN, stool guaiac if concern)
   inputs: sbp, creatinine, potassium
   actions: panel.cardiac, panel.renal
   advance: BP at target + AKI improving + electrolytes normal + alternative pain control adequate
10. 10FOLLOWUP
    NSAID-AVOIDANCE COUNSELING: comprehensive education on NSAID risks for patient + family + caregivers + PCP + pharmacy team; identify all OTC sources (ibuprofen, naproxen, aspirin >1 g, combination products); MEDICATION-LIST DOCUMENTATION: "NSAID-AVOID" added to allergy list with rationale; ALTERNATIVE PAIN REGIMEN: acetaminophen 1 g PO q6h max 3-4 g/d for general pain (max 2 g/d if cirrhosis), topical NSAID (diclofenac gel, lidocaine patch — minimal systemic) for localized musculoskeletal, duloxetine 30-60 mg PO daily for chronic musculoskeletal, intra-articular steroid for joint-specific, gabapentinoid 100-300 mg TID for neuropathic, opioid for severe acute pain only with multimodal + opioid stewardship; PCP COORDINATION: weekly BP + BMP × 4 weeks then monthly during recovery; KIDNEY RECOVERY: nephrology follow-up in 1-2 weeks for post-AKI surveillance, baseline eGFR re-establishment (some never fully recover after triple-whammy AKI); CV RISK ASSESSMENT: if previously on selective COX-2 for chronic pain, reassess CV risk + consider class avoidance; ALL CARE TEAMS: pharmacy alert on chart "NSAID-AVOID — drug-induced HTN crisis"; PCP + cardiology + nephrology + pain medicine follow-up within 1-2 weeks
    advance: NSAID-avoid alert documented + alternative pain regimen prescribed + PCP/cardiology/nephrology/pain medicine follow-up booked + patient + family education done