394.3 ð©º å §ç§å°ç§èåç
394.3.0.1 ð äžé éé»
- 22E updates:
- Copeptin (CT-proAVP) â stable surrogate for AVP; hypertonic saline + copeptin test å¯å代 traditional water deprivation
- Tolvaptan: V2 antagonist FDA approved for SIADH + ADPKD; LFT monitoring (hepatotoxicity); 30-day limit in some indications
- Renaming: ICRP suggests âAVP-Dâ (deficiency) and âAVP-Râ (resistance) instead of âcentral / nephrogenic DIâ â 22E mostly still uses DI terminology
- ICI-related posterior pituitary involvement uncommon (anterior more common)
- Taiwan: å¥ä¿ desmopressin (oral, intranasal) for CDI; thiazide / amiloride for NDI; tolvaptan æ¢ä»¶
394.3.0.2 ð Pearls (15)
394.3.0.2.1 Diagnosis
- Copeptin > 4.9 pmol/L after hypertonic saline â primary polydipsia (rules out CDI)
- Direct copeptin > 21.4 pmol/L without stim â CDI / NDI confirmed
- Water deprivation test still useful but copeptin gaining ground
- MRI bright spot absent â CDI confirmed; sometimes éšå cases ä» has it
- Stalk thickening â workup for granulomatous (sarcoid, LCH), germinoma, IgG4-RD, hypophysitis
394.3.0.2.2 SIADH Management
- Tolvaptan: V2 antagonist; aquaresis without Na loss; LFT monitoring; 30-day limit some indications; expensive
- Conivaptan: IV V1a + V2 antagonist; acute use only
- Salt tablets + loop diuretic combo: increases free water clearance
- Demeclocycline: induces NDI; rarely used now (nephrotoxicity)
- Urea oral: osmotic; well tolerated; 22E option
394.3.0.3 ð Taiwan + å¥ä¿
394.3.0.3.1 CDI
- å¥ä¿ desmopressin (Minirin):
- Intranasal spray
- Oral tablet
- SC injection (peri-op)
- å¥ä¿ vasopressin tannate (older, replaced)
- MRI sella + stalk imaging å¥ä¿
394.3.0.4 ð å §å°å¿ æ (15)
- åŸèè§£å + ADH/oxytocin
- ADH V1/V2/V3 receptors + ååèœ
- SIADH Bartter-Schwartz criteria + æé€åå¿ é å thyroid/adrenal
- SIADH causes 8 å€§é¡ (paraneoplastic, CNS, pulmonary, drug, nausea/pain, hypothyroid/AI, HIV, hereditary)
- CSW vs SIADH éå¥ (volume status critical!)
- Acute hypoNa correction protocol + ODS prevention
- Re-lowering Na technique for over-correction
- CDI vs NDI + water deprivation + copeptin
- CDI causes (idiopathic, tumor, surgery, TBI, infiltrative, genetic)
- NDI causes (lithium #1, hypercalcemia, hypokalemia, genetic V2/AQP2)
- Wolfram syndrome (DIDMOAD)
- Pregnancy DI (placental vasopressinase)
- Triphasic post-pituitary surgery + management each phase
- Tolvaptan, conivaptan indications + LFT
- 22E: copeptin, AVP-D/AVP-R nomenclature, urea, ICRP guideline
394.3.0.5 âïž Detailed Hyponatremia Workflow
1. Plasma Osm
- Normal/high (pseudo-/iso-/hyperosmolar) â not true hypoNa
- Low (true hypotonic hypoNa) â continue
2. Volume status
- Hypovolemic: GI loss, diuretic, salt-wasting
- Euvolemic: SIADH, hypothyroidism, AI, primary polydipsia
- Hypervolemic: HF, cirrhosis, nephrosis
3. Urine Na
- < 20: extra-renal (diarrhea, vomiting)
- > 20: renal (diuretic, AI, salt-wasting, SIADH)
4. Urine Osm
- < 100: primary polydipsia, beer potomania, "tea + toast"
- > 100: SIADH, AI, hypothyroidism
5. æ secondary AI (cortisol stim) + thyroid (TSH)
6. SIADH Bartter-Schwartz
394.3.0.6 âïž Severe SIADH (Na < 120 + symptomatic) â å §å° step-by-step
1. ABCs + IV access
2. 3% saline 100 mL IV over 10 min (or 2 mL/kg)
3. Repeat à 1-2 if ä» seizing / ç¥ç¶æ¡å
4. Goal: â Na 4-6 mmol/L within 6 h
5. After symptoms relief, slow correction
6. 24h max â 8-10 (chronic) or 12 (acute < 48h)
7. Q2h Na monitoring initially
8. If over-correction â D5W + desmopressin (re-lower)
9. Long-term: fluid restrict 800-1000 mL/d, treat cause
10. If cabal: tolvaptan / urea / salt + loop diuretic
394.3.0.7 âïž Triphasic Post-Pituitary Surgery (CDI/SIADH/CDI)
Phase 1 (Day 0-5): CDI
- Stalk damage â ADH äžèœ release
- Polyuria + thirst + é« Na
- Treat: small DDAVP doses; allow thirst-driven fluid intake
Phase 2 (Day 5-10): SIADH
- Stored ADH released uncontrolled from damaged neurons
- HypoNa, water retention
- Treat: STOP DDAVP; fluid restrict; sometimes 3% saline if severe
Phase 3 (after Day 10): permanent CDI
- If neurons die, permanent ADH lack
- Treat: chronic DDAVP
- äœæäº phase 1 alone resolves (transient CDI 50%)
â ïž Recognition essential â wrong-direction therapy is dangerous