At 72 h postburn, the wound tissue comes into a phase of rejection reaction, which is a response of the viable tissues due to disintegration of necrotic tissue and cells in the interface of the lesion area. 

Usually mixed and extensive, this reaction process primarily includes three patho-geneses: 

(1) the disintegration of necrotic histiocytes in the injury interface; 

(2) the regeneration of viable histio-cytes in the interface of the lesion area; 

(3) microbial infection in the injury interface. 

Besides an inflammatory reaction, disintegration of necrotic histiocytes may induce cell liquefaction in the injury interface and, more importantly, the accumulation of cell liquefied products continues the aggravation of the injured tissue. 

Meanwhile, the residual viable tissues in the injury interface begin instinctive regeneration when disintegrated tissues develop into a destructive substance unfavorable to the environment of cell regeneration, thereby inducing serious inflammation. 

The combination of the two above pathogeneses disturbs flora residing in the skin and causes the destruction of microbes in the injured area, both of which further aggravate damage and may result in systemic injury at any time. 

This process is called ‘rejection injury of necrot-ic tissues’, and is the last primary injury of a burns wound.