Liquefactive necrosis

Liquefactive necrosis

Liquefactive necrosis (or colliquative necrosis) is a type of necrosis which results in a transformation of the tissue into a liquid viscous mass.[1] Often it is associated with focal bacterial or fungal infections. In liquefactive necrosis, the affected cell is completely digested by hydrolytic enzymes, resulting in a soft, circumscribed lesion consisting of pus and the fluid remains of necrotic tissue. Dead leukocytes will remain as a creamy yellow pus.[2] After the removal of cell debris by white blood cells, a fluid filled space is left. It is generally associated with abscess formation and is commonly found in the central nervous system.

In the brain

For unclear reasons, hypoxic death of cells within the central nervous system also results in liquefactive necrosis.[3] This is a process in which lysosomes turn tissues into soup as a result of lysosomal release of digestive enzymes. Loss of tissue architecture means that the tissue is essentially liquefied. This process is not associated with bacteria action or infection.

The affected area is soft with liquefied centre containing necrotic debris. Later, a cyst wall is formed.

Microscopically, the cystic space contains necrotic cell debris and macrophages filled with phagocytosed material. The cyst wall is formed by proliferating capillaries, inflammatory cells, and gliosis (proliferating glial cells) in the case of brain and proliferating fibroblasts in the case of abscess cavity.

In the lung

Liquefactive necrosis can also occur in the lung.[4][5]


  1. ^ Robbins and Cotran: Pathologic Basis of Disease, 8th Ed. 2010. Pg. 15
  2. ^ Robbins and Cotran: Pathologic Basis of Disease, 8th Ed. 2010. Pg. 15
  3. ^ Robbins and Cotran: Pathologic Basis of Disease, 8th Ed. 2010. Pg. 15
  4. ^ "Cell Injury". Retrieved 2009-05-15. 
  5. ^ Quaia E, Baratella E, Pizzolato R, Bussani R, Cova MA (March 2009). "Radiological-pathological correlation in intratumoural tissue components of solid lung tumours". Radiol Med 114 (2): 173–89. doi:10.1007/s11547-008-0354-6. ISBN 1154700803546. PMID 19082781. 

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