Cyanide poisoning

Cyanide poisoning is a cause of an acute anoxic-ischemic encephalopathy that also has eventual chronic sequelae.


Acute cyanide poisoning is rare and often occurs after suicidal oral ingestion of cyanide-containing compounds, however there are other sources such as after smoke inhalation . Chronic cyanide poisoning is generally related to occupational exposure, such as working in the metal industry .

Clinical presentation

Patients can present with a variety of devastatingly disabling clinical features, often manifesting within minutes of exposure :

  • headache
  • seizures
  • agitation
  • cardiac arrhythmias
  • cardiac and respiratory arrest, often leading to coma and rapid death

If a patient survives the acute poisoning, eventual chronic neurological sequelae include the development of movement disorders (e.g. parkinsonism, choreoathetosis, dystonia), or rarely, the development of memory impairment .


A cyanide is a compound, known simply as a 'cyanide', that contains a cyanide group (CN) . These compounds include solids, typically cyanide salts (e.g. potassium cyanide), liquids or gases (e.g. hydrogen cyanide), which can cause toxicity through ingestion, dermal absorption, or inhalation . It is highly toxic, with the mean lethal dose of potassium cyanide only being 3 mg/kg .

Cyanide is a respiratory chain metabolism toxin that inhibits the mitochondrial enzyme cytochrome c oxidase, a terminal enzyme of the respiratory electron transport chain . This culminates in cytotoxic anoxia in cells, especially those that have high oxygen requirements . In the brain, the structures that require the highest oxygen requirement, namely the basal ganglia and cerebral cortex, are the regions most prominently affected by this anoxic toxicity . Thus, the basal ganglia undergoes hemorrhagic necrosis and the cortex undergoes pseudolaminar necrosis . Notably and unusually, despite its rich oxygen supply, the hippocampi are characteristically spared in this process .

Radiographic features

Cyanide poisoning characteristically tends to bilaterally affect the basal ganglia, especially the striatum, and the cerebral cortex, especially the sensorimotor cortex . However, in severe cases that lead to rapid death, more widespread changes, including diffuse cerebral edema, can be seen .


Classically seen as hypo-attenuation bilaterally in the basal ganglia, reflective of necrosis. These areas may or may not have evidence of hyper-attenuating macroscopic hemorrhage . Cortical changes are often not evident on CT .


Regions of involvement are identical to those involved on CT, but are appreciated in greater detail. Signal characteristics of the necrosis in the acute setting include :

  • T1: generally high signal, consistent with pseudolaminar necrosis when affecting the cortex, but also due to presence of hemorrhage
  • T2/FLAIR: affected areas demonstrate high signal that become more pronounced within weeks
  • T1 C+ (Gd): usually vivid contrast enhancement
  • DWI: affected areas show increased diffusion signal

In the chronic phase after acute cyanide poisoning, a decrease of high signal intensity in all sequences is generally appreciated, but this may take more than a year to occur . Unlike other toxic encephalopathies, such as methanol poisoning, cystic sequelae usually do not eventuate .

Treatment and prognosis

Treatment generally involves administration of antidotes such as hydroxycobalamin, which binds to cyanide compounds to create non-toxic compounds that can be safely excreted by the kidneys . Another commonly used antidote is sodium thiosulphate, which accelerates the metabolism of cyanide is more benign molecules .

The prognosis of acute cyanide poisoning is very grim, with a 95% mortality rate .

Differential diagnosis

For involvement in and around the basal ganglia, consider: