Organophosphorus nerve agents (OPNA) are the most dangerous chemical warfare agents known. They are an immense threat acting as potent irreversible cholinesterase inhibitors in the nervous system. OPNA induce an immediate hypercholinergic activity responsible for most of the initial toxidrome. During intoxications with high sublethal to lethal doses of OPNA, the excess of acetylcholine in the brain triggers seizures and leads to secondary recruitment of the excitatory glutamate system. Through overstimulation of its receptors, including the ionotropic N-methyl-D-aspartate receptors (NMDAR), glutamate is thought to play a prominent role in the long-lasting maintenance of seizure activity, status epilepticus (SE), and the development of seizure-related brain damage. Ketamine is a NMDAR antagonist clinically used in many medical areas. Despite numerous preclinical and clinical publications reporting ketamine’s promising properties, the agent is still not widely recognized as a treatment for epileptic conditions. Indeed, when combined with other antiepileptic drugs, it may terminate seizures and prevent neuronal damage and neurobehavioral deficits even when seizures have evolved into refractory SE. In this narrative review, we discuss the data on OPNA-related SE and treatment approaches with ketamine published since 2017. Some standardization of the preclinical models used to evaluate the efficacy of ketamine in OPNA poisoning is recommended along with the use of non-rodent models. Because OPNA-induced SE finally shares many similarities with SE of other origins, randomized clinical trials on ketamine for treatment of SE may facilitate its promotion as a therapeutic approach combined with other drugs to improve the management of casualties with OPNA intoxication.