Guardat en:
| Autor principal: | |
|---|---|
| Format: | Recurso digital |
| Idioma: | |
| Publicat: |
Zenodo
2026
|
| Matèries: | |
| Accés en línia: | https://doi.org/10.5281/zenodo.19776961 |
| Etiquetes: |
Afegir etiqueta
Sense etiquetes, Sigues el primer a etiquetar aquest registre!
|
Taula de continguts:
- <p><strong>Background:</strong> Neonatal metabolic alkalosis (MetAlk), though less studied than acidosis, carries significant morbidity — impaired oxygen delivery, cardiac arrhythmias, electrolyte disturbance, and post-operative respiratory risk in conditions such as infantile hypertrophic pyloric stenosis.</p> <p><strong>Framework:</strong> MetAlk requires two compulsory components — generation (H⁺ loss/HCO₃⁻ gain) and maintenance (impaired renal HCO₃⁻ excretion). The kidney cannot excrete excess HCO₃⁻ without Cl⁻. Restoring chloride — not administering acid — is the cornerstone of treatment in the majority of cases.</p> <p><strong>Classification:</strong> Spot urine chloride (<20 vs >20 mEq/L) differentiates chloride-responsive from chloride-resistant MetAlk, driving the entire treatment algorithm. Furosemide timing and borderline values require clinical interpretation.</p> <p><strong>Key Message:</strong> Six concurrent pillars (stop generation; restore Cl⁻; restore K⁺ as KCl only; restore volume; disease-specific Rx; pharmacological agents) address all maintenance mechanisms. Acetazolamide is first-line pharmacological therapy for refractory cases. HCl 0.1N (central line only) and arginine HCl (peripheral) are reserved for severe refractory alkalosis.</p>