BackgroundThere is currently conflicting evidence surrounding the effects of obesity on postoperative outcomes. Previous studies have found obesity to be associated with adverse events, but others have found no association. The aim of this study was to determine whether increasing body mass index (BMI) is an independent risk factor for development of major postoperative complications.MethodsThis was a multicentre prospective cohort study across the UK and Republic of Ireland. Consecutive patients undergoing elective or emergency gastrointestinal surgery over a 4‐month interval (October–December 2014) were eligible for inclusion. The primary outcome was the 30‐day major complication rate (Clavien–Dindo grade III–V). BMI was grouped according to the World Health Organization classification. Multilevel logistic regression models were used to adjust for patient, operative and hospital‐level effects, creating odds ratios (ORs) and 95 per cent confidence intervals (c.i.).ResultsOf 7965 patients, 2545 (32·0 per cent) were of normal weight, 2673 (33·6 per cent) were overweight and 2747 (34·5 per cent) were obese. Overall, 4925 (61·8 per cent) underwent elective and 3038 (38·1 per cent) emergency operations. The 30‐day major complication rate was 11·4 per cent (908 of 7965). In adjusted models, a significant interaction was found between BMI and diagnosis, with an association seen between BMI and major complications for patients with malignancy (overweight: OR 1·59, 95 per cent c.i. 1·12 to 2·29, P = 0·008; obese: OR 1·91, 1·31 to 2·83, P = 0·002; compared with normal weight) but not benign disease (overweight: OR 0·89, 0·71 to 1·12, P = 0·329; obese: OR 0·84, 0·66 to 1·06, P = 0·147).ConclusionOverweight and obese patients undergoing surgery for gastrointestinal malignancy are at increased risk of major postoperative complications compared with those of normal weight.

1. Platelet and fibrinogen survival have been studied by isotope tagging in normal and abnormal states of coagulation in humans and dogs. 2. By our technic, the normal curve of platelet survival is exponential. Evidence is given that such a curve is obtained because of random utilization of the platelets in the continuous process of coagulation. 3. In the postoperative subject and in the subject receiving epinephrine injections, platelet survival is shortened because the process of coagulation is speeded up. In the hypocoagulable, the curve of platelet survival becomes more nearly linear because random platelet destruction ceases. 4. When a massive thrombus forms, platelet survival is shortened. Evidence is given that this may be due to escape of thrombin from the clot into the systemic circulation—with a resultant hypercoagulable state. 5. Fibrinogen survival was not altered in those states in which increased platelet utilization occurred. This is explained by the theory that the alteration in the hemostatic mechanism had not penetrated to the fibrinogen-fibrin stage. 6. Hypercoagulability is defined as that state in which platelet utilization is accelerated—whether or not thrombosis occurs.

We describe the case of a three-year-old girl with Wilms' tumor, whose serum showed at least a fivefold increase in relative viscosity although concentrations of albumin and immunoglobulins were normal. An unusual electrophoretogram of serum protein prompted further investigation. The increased viscosity was caused by the presence of high concentrations of hyaluronic acid, a glycosaminoglycan normally not detectable in serum.

There is much evidence favoring the concept of coagulation as a continuous process in the normal subject. In order to learn more about the dynamics of this process, we have been studying the survival of physiological amounts of the various clotting factors in the normal subject. With the development of isotope labeling, it has for the first time become possible to carry out such studies. We (1-3) and others (1-10) have applied this technique to studies of platelet and fibrinogen turnover. These studies were possible because both platelets and fibrinogen are present in large amounts and can be separated in relatively pure form. Isotope techniques have not yet been applied to a study of the other proteins involved in coagulation because they are present in relatively trace amounts and cannot yet be isolated in sufficiently pure form.In order to overcome these problems, we have developed a technique of in vivo labeling, separating, and counting two of the clotting proteins, Factor VIII (antihemophilic globulin) as an example of a protein consumed during coagulation and Factor IX (plasma thromboplastin component, Christmas factor) as an example of a clotting protein not consumed during coagulation. Three mc of S"-DL-methionine was inj ected intravenously into suitable humans. Subj ects were selected who had no evidence of liver disease or of bleeding tendency. The labeled amino acid was used by the recipient in the formation of plasma proteins. The more rapid the turnover of the protein, the higher the specific activity would be. Twenty-four hours later, the subject was phlebotomized. ACD solution was used as anticoagulant, and 500 ml of blood was obtained with as little trauma as possible. The blood was immediately infused into the normal human recipients in whom the survival of the labeled protein was to be followed.Separating labeled proteins. This was accomplished by immunological methods.A partially purified Factor VIII preparation was made from human plasma by the method of Spaet and Kinsell (11). This mixture of proteins was made into a 10% solution with distilled water and mixed in a 1:1 suspension with Freund adjuvant.2 The mixture was injected intramuscularly twice a week for a period of 2 months into a group of twelve rabbits. After a 10-day rest period, the rabbits each received an iv injection of 3 ml of an alum-precipitated preparation made from a 5% solution of the original partially purified Factor VIII preparation. Seven days later, the rabbits were bled into 0.1 vol of 0.1 M sodium oxalate, the plasmas were separated and pooled, and 0.1 vol of 0.1% aqueous merthiolate was added.Blood was drawn from a patient with hemophilia whose Factor VIII level when measured by the partial thromboplastin technique (12) was less than 1%. This blood was drawn into 0.1 vol of 0.1 M sodium oxalate, and 0.1 vol of 0.1%So aqueous merthiolate was added.