This is an open access article under the terms of the Creat ive Commo ns Attri bution-NonCo mmercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

Pediatric acute-onset neuropsychiatric syndrome is a clinical concept used to describe a subgroup of children with sudden onset of psychiatric and somatic symptoms. The diagnostic term and especially management of children differs depending on the clinical setting to which they present, and the diagnosis and management is controversial. The aim of this paper is to propose a clinical guidance including homogenous diagnostic work-up and management of paediatric acute onset neuropsychiatric syndrome within the Nordic countries. The guidance is authored by a Nordic-UK working group consisting of paediatric neurologist, child psychiatrists and psychologists from Denmark, Norway, Sweden and Great Britain, and is the result of broad consensus. Conclusion: Consensus was achieved in the collaboration on work-up and treatment of patients with paediatric acute-onset neuropsychiatric syndrome, which we hope

The elimination of iodine‐labelled fibrinogen was followed in 3 groups of dogs after: 1. thromboplastin infusion, 2. simultaneous infusions of thromboplastin and epsilon aminocaproic acid (EACA), and 3. simultaneous infusions of thromboplastin and Trasylol. Platelet count, fibrinogen concentration, radioactivity in plasma and in fibrinogen as well as hematocrit were determined. Thromboplastin caused changes of the same type as those previously obtained with thrombin, indicating the development of a fibrinolytic process, secondary to intravascular coagulation. The secondary changes were effectively blocked by pretreatment with EACA and Trasylol. The incidence of and mortality in thromboembolism suggest some anticoagulant effect of Trasylol. The antifibrinolytic activity of Trasylol is much stronger than the anticoagulant one. EACA too, seems to give some protection against thromboplastin‐induced coagulation.