Early recognition of the disease and implementation of appropriate treatment are very important here, as the symptoms occur suddenly and the progression of the disease is very rapid and, even in a few hours, can lead to death.

The aetiology of this disease is not fully understood, although doctors' observations have shown its connection with viral infections, after which Reye's syndrome has its origin. A link has also been noted between the development of the disease and the administration of aspirin, salicylates or anti-diarrhoeal drugs.

The main symptoms of the syndrome are encephalopathy and fatty degeneration of the liver. There is damage to the mitochondria, which begin to swell causing swelling of the brain and fatty infiltration of the liver, kidneys and heart. Blood ammonia levels also rise, due to the disruption of the mechanisms for converting ammonia into urea.

The first symptoms are nausea, lethargy, confusion, slowed ECG and liver dysfunction. In stage II, aggression, inadequate response to pain, hallucinations and liver function impairment occur. Stage III includes coma and hyperventilation with preservation of eye and pupil reflexes. When eye reflexes cease, we can speak of stage IV. In it, the patient falls into a deepened coma, the rigidity worsens, and brainstem damage occurs. The last, stage V, is characterised by seizures, muscle flaccidity and, finally, respiratory arrest. Investigations in the development of the disease show elevated levels of ammonia and amintransferase in liver tests. On the side of the coagulation system, prolongation of the prothrombin time is noted.[1]