Cocaine (koe kane') is a potent local anesthetic that appears to act by inhibition of voltage-gated sodium channels, increasing the threshold for electric excitability of nerve axons and thus decreasing neuroconduction. In the central nervous system, cocaine appears to block both norepinephrine and serotonin reuptake. The aim of this study is to determine the histological effect of crack cocaine on the liver of adult albino wistar rat. A total of forty (40) adult Albino Wistar rats of comparable sizes were used for this study. They were divided into four equal groups (A – D) with ten (10) rats each. Group A served as the control and the rats were given distilled water and feed only. In addition to feed and water, groups B rats were given 0.5ml (100mg) crack cocaine extract and crack cocaine extract, group C rats were given 2ml (200mg) crack cocaine extract, and group D rats were given 5ml (300mg) crack cocaine extract respectively. The drug administration was given daily for 14 days (2 weeks) and the weights of both the test and control animals was monitored before and after administration of crack cocaine extract. The administration of the crack cocaine extracts was given orally. After the administration, the rats were put under light chloroform anaesthesia and the liver were obtained. ANOVA was used to analyze the results of the weight and differences was considered significant at p<0.05 level of confidence. All data was expressed in table as mean ± standard deviation (SD). The results of this study show presence of bridging necrosis and portal fibrosis in the liver histology of test wistar rats administered with crack cocaine at 200 and 300mg when compared with the non-cocaine administered group also a non-significant variation was observed in the body weight of control and test groups across the groups. In conclusion, the use of cocaine can lead to significant and harmful effects on liver histology, resulting from a combination of factors related to the drug's pharmacological actions, metabolism, and physiological responses. These changes stem from cocaine's vasoconstrictive properties, generation of reactive metabolites, direct toxic effects, and interactions with other substances.