Asthma is one of the most common chronic respiratory diseases, present in all age groups, characterized by inflammation and narrowing of the airways. Mucoid impactions (MI) play a key role in fatal asthma and in airway obstruction in patients with severe asthma. MI in asthma patients consist of mucus, fibrin, and various inflammatory cells. Mucus production is the central cause of MI formation. Mucus produced in type 2 asthma shows a significantly higher modulus of elasticity, making it much more viscous and difficult to expectorate, contributing to MI formation. The main mucins in the lungs, MUC5B and MUC5AC, determine the viscoelastic properties of the mucus based on their mutual ratio. Eosinophils, the dominant cells in type 2 inflammation associated with asthma, contribute to MI formation by releasing pro-inflammatory cytokines, cytotoxic proteins, and oxidants that damage the epithelium and increase mucus viscosity. EETosis, the process of forming eosinophilic extracellular traps (EET), further exacerbates the situation by creating Charcot-Leyden crystals that alter the physical properties of the mucus. Recent studies have highlighted the key role of neutrophils in the formation of mucoid impactions, especially in severe asthma. Neutrophils are often found in greater numbers in the sputum of patients with severe asthma, contributing to inflammation by releasing pro-inflammatory cytokines and abnormal activity of the NLRP3 (NOD-like receptor protein 3) inflammasome, forming neutrophil extracellular traps (NETs), and lipoxins. Mucoid impactions can cause airway obstruction, leading to dyspnea, reduced blood oxygenation and an increased risk of bacterial infections. Hydration, air humidification, and flexible bronchoscopy are key steps in initial treatment, while biological drugs like benralizumab significantly reduce the number of mucoid impactions. New mucolytics such as tris (2-carboxyethyl) phosphine (TCEP) also show promising results in mucus breakdown and clearance improvement.