The current social communication domain criteria for autism diagnosis require individuals to have deficits across three social skills: social-emotional reciprocity, nonverbal communication, and developing and sustaining relationships. Communication deficits are due to problems with social-emotional skills like joint attention and social reciprocity.A range of social-emotional reciprocity difficulties (an individuals ability to naturally engage in social interactions) may be present. Autistic individuals may lack mutual sharing of interests, for example many autistic children prefer not to play or interact with others. They may lack awareness or understanding of other peoples thoughts or feelings – a child may get too close to peers (entering their personal space) without noticing that this makes them uncomfortable. They may also engage in atypical behaviors to gain attention, for example a child may push a peer to gain attention before starting a conversation.Older children and adults with ASD perform worse on tests of face and emotion recognition than non-autistic individuals, although this may be partly due to a lower ability to define a persons own emotions.Autistic people experience deficits in their ability to develop, maintain, and understand relationships, as well as difficulties adjusting behavior to fit social contexts. ASD presents with impairments in pragmatic communication skills, such as difficulty initiating a conversation or failure to consider the interests of the listener to sustain a conversation. The ability to be focused exclusively on one topic in communication is known as monotropism, and can be compared to "tunnel vision".
Liver failure  is the inability of the liver to perform its normal synthetic and metabolic functions as part of normal physiology. Two forms are recognised, acute and chronic (cirrhosis). Recently, a third form of liver failure known as acute-on-chronic liver failure (ACLF) is increasingly being recognized. Acute
Acute liver failure is defined as "the rapid development of hepatocellular dysfunction, specifically coagulopathy and mental status changes (encephalopathy) in a patient without known prior liver disease". :1557The disease process is associated with the development of a coagulopathy of liver aetiology, and clinically apparent altered level of consciousness due to hepatic encephalopathy. Several important measures are immediately necessary when the patient presents for medical attention. The diagnosis of acute liver failure is based on a physical exam, laboratory findings, patient history, and past medical history to establish mental status changes, coagulopathy, rapidity of onset, and absence of known prior liver disease respectively. :1557The exact definition of "rapid" is somewhat questionable, and different sub-divisions exist, which are based on the time from onset of first hepatic symptoms to onset of encephalopathy. One scheme defines "acute hepatic failure" as the development of encephalopathy within 26 weeks of the onset of any hepatic symptoms. This is sub-divided into "fulminant hepatic failure", which requires onset of encephalopathy within 8 weeks, and "subfulminant", which describes onset of encephalopathy after 8 weeks but before 26 weeks. Another scheme defines "hyperacute" as onset within 7 days, "acute" as onset between 7 and 28 days, and "subacute" as onset between 28 days and 24 weeks.