A research study of 400 adult patients emerging from general anesthesia in the PACU were assessed for delirium using the Confusion Assessment Method for the ICU (CAM-ICU) found rates of emergence delirium of 31% at PACU admission with rates declining to 8% by 1 hour. References
Further reading
Vlajkovic GP, Sindjelic RP (Jan 2007). "Emergence delirium in children: many questions, few answers". Anesth. Analg. 104 (1): 84–91. doi:10.1213/01.ane.0000250914.91881.a8. PMID 17179249. S2CID 7315961. Lepouse C, Lautner CA, Liu L, Gomis P, Leon A (Jun 2006). "Emergence delirium in adults in the post-anaesthesia care unit". Br. J. Anaesth. 96 (6): 747–53. doi:10.1093/bja/ael094. PMID 16670111. == External links ==
The nucleotide substitutions were discovered in the late 1990s by classical linkage analysis and are now known as p.R122H and p.N29I respectively, according to the amino acid substitution and position in the protein sequence. These mutations are rarely identified in general screens of patients with idiopathic disease and the phenotype of p.R122H and p.N29I is now well characterised with the p.A16V mutation recently characterised for the first time. There are many other rare mutations or polymorphisms of PRSS1 which remain less well understood and not all HP families have had the responsible genetic mutation identified. The mechanism by which these genetic mutations cause pancreatitis is not yet known; but is likely to be the result of increased autoactivation or reduced deactivation of trypsinogen. However, a novel mechanism has recently been identified in a p.R116C kindred. Diagnosis
Families are defined as having HP, if the phenotype is consistent with highly penetrant autosomal dominant inheritance. In simple terms, this would require two or more first degree relatives (or three or more second degree relatives) to have unexplained recurrent-acute or chronic pancreatitis in two or more generations. It is an autosomal dominant disease with penetrance that is generally accepted to be ≈80%. Management
Treatment of HP resemble that of chronic pancreatitis of other causes. Treatment focuses on enzyme and nutritional supplementation, pain management, pancreatic diabetes, and local organ complications, such as pseudocysts, bile duct or duodenal obstruction. (PMC1774562)

Prognosis
A 2009 study which followed 189 patients found no excess mortality despite the increased risk of pancreatic cancer. References


== External links ==