Pulmonary alveolar proteinosis (PAP) is characterized by accumulation of surfactant in the alveoli due to impaired clearance or overproduction leading to progressive dyspnea and potentially fatal respiratory failure. This review provides a comprehensive analysis of current and emerging therapeutic strategies for PAP, evaluating their pathophysiological rationale, clinical efficacy and limitations. A structured literature review was conducted using PubMed, Google Scholar, and Cochrane Library databases to identify studies published between 01.01.2002 and 01.07.2026. Search terms included: “PAP,” “whole lung lavage (WLL),” “segmental lung lavage (SLL),” “granulocyte-macrophage colony-stimulating factor (GM-CSF),” “molgramostim,” “sargramostim,” “rituximab,” and “statin therapy.” WLL removes accumulated surfactant, but it remains hindered by its invasive nature, procedural risks, and recurrence rates requiring repeated sessions. To overcome these limitations, less invasive techniques, such as mini-WLL and bronchoscopic SLL, achieve targeted surfactant clearance with reduced volume load, making them valuable alternatives for high-risk patients or bridging therapies. Targeted pharmacotherapies including inhaled recombinant GM-CSF which restores alveolar macrophage clearance functions, improves gas exchange and reduces the reliance on WLL. Statin therapy may reduce macrophage lipid accumulation. Despite these interventions rituximab, extracorporeal membrane oxygenation (ECMO) support, or lung transplantation may be useful in selected cases. Innovations, including gene therapy and gene-corrected macrophage transplantation, aiming to permanently restore cellular function are also being tested. The management of PAP is shifting from global mechanical surfactant removal towards personalized, local lavage or pathogenetically driven pharmacological algorithms, however WLL remains essential for acute rescue in severe hypoxemia.