Ann R Coll Surg Engl 2006; 88: 610-616 610In the modern era, patients with obstructive jaundice can expect to be operated on with a low mortality and their morbidity can be reduced by relatively simple clinical interventions. 1 This review provides a literature-based guide to the optimal management of the patient with obstructive jaundice with emphasis placed on prevention of complications.
MethodologyA search of the Pubmed database was performed using the keywords of: obstructive jaundice, complications, biliary drainage, renal failure, bactobilia, coagulation, coagulopathy and vitamin K . All studies and reviews that addressed the topic were analysed by the authors and classified according to their methodology as retrospective, prospective, descriptive or comparative. Tables were generated to summarise the relevant articles.
Results
Coagulation overviewEfficient coagulation is initiated by platelet adhesion and aggregation, which activates the coagulation cascade. The process consists of an extrinsic and intrinsic pathway of inactivate pro-enzymes, pro-and anticoagulants which, when activated, form thrombin. Vitamin K is an essential co-factor for the synthesis of the procoagulant fat-soluble factors II, VII, IX and X. as well as the anticoagulant factors protein C, protein S and anti-thrombin III.Vitamin K is present in green vegetables and is synthesised in the gut by luminal bacteria. Absorption is dependent on the presence of luminal bile salts and the daily requirement of vitamin K is about 1 µ g/kg. The liver synthesises all the vitamin Kdependent procoagulant and anticoagulant factors. In obstructive jaundice, mal-absorption of vitamin K results in hypoprothrombinaemia and a fall in the concentration of the other vitamin K-dependent pro-and anticoagulation factors.Laboratory assays are used to assess the state of the coagulation system. The prothrombin time expressed as the international normalised ratio (INR) and measures the vitamin K-dependent factors VII, X, prothrombin and fibrinogen levels as well as Factor V. This is the extrinsic and the common pathway. Prolongation of prothrombin time has been used to gauge the extent of vitamin K deficiency although a normal prothrombin time may mask a subclinical deficiency of vitamin K. 2 The activated partial thromboplastin time is used to monitor heparin therapy and measures the efficacy of Factors V, VIII, IX, X, XI and XII, prothrombin and fibrinogen and von Willebrand's factor.
Management of the coagulopathy associated with obstructive jaundiceAlthough the predominant defect in the hypocoaguable state associated with obstructive jaundice is the mal- absorption of vitamin K, the pathogenesis is frequently multifactorial. 2 A combination of hepatocyte dysfunction and endotoxaemia may result in wide-spread microthrombosis and the triggering of the intrinsic cascade precipitating disseminated intravascular coagulation. Prevention is achieved by administering parenteral vitamin K which will correct the deficiency in those without chronic liver disease. 2 Pat...