The sequence of events in haematogenous metastasis from colonic carcinoma was analysed, using 1541 necropsy reports from 16 centres. The findings are consistent with the cascade hypothesis that metastases develop in discrete steps, first in the liver, next in the lungs and finally, in other sites. Deviations of necropsy findings from the cascade model are largely explained on the basis of false negative reports. In only 216 of 1194 cases was there suggestive evidence that metastatic patterns (excluding lymph nodes) were causally related to lymphatic or non-haematogenous pathways. The incidence of metastatic involvement in 'other' (quaternary) sites correlated with target organ blood-flow (ml min-) per g, only when bone marrow and thyroid were excluded. In the thyroid the incidence was lower than expected on the basis of blood flow per g tissue; this may indicate that the thyroid is an unfavourable site for metastatic growth of colonic carcinoma. In the bone marrow it is higher; the latter may be due to delivery of cancer cells via both arterial blood and the vertebral venous plexus. Recognition of this pattern of metastases in the bone marrow could be important with respect of diagnosis and therapy, in patients with colonic carcinoma.

SUMMARY In a prospective necropsy study of the large bowel in 365 cases, the commonest polyp identified was the hyperplastic (metaplastic) variety, of which 86. 1% of the total were located in the rectum. The other main type of polyp found, and of much greater importance because of its malignant potential, was the neoplastic adenoma. These were present, either singly or multiply, in 73 of 198 male cases (36.9%) and in 48 of 167 female cases (28.7%). Their prevalence and their tendency to be multiple rose with increasing age in both sexes. Most adenomas had a tubular growth pattern and 88.8% of these were under 1 cm in diameter. There was a fairly even distribution of adenomas throughout the large bowel but a higher proportion of adenomas over 1 cm in diameter occurred in the caecum, sigmoid colon, and rectum than at other sites. In the whole series nine adenocarcinomas were present, two of which were arising in adenomas.There is much clinical, experimental, and pathological evidence that the vast majority of carcinomas of the large bowel arise from adenomas, a process referred to as the adenoma-carcinoma sequence.1 The only obvious exception to this is in the case of cancer arising in long-standing ulcerative colitis, where the precursor dysplastic lesion is not a discrete polyp, but often affects a wide area of the bowel, which macroscopically may be flat or have a poorly circumscribed velvety or nodular appearance.Whereas there is a mass of information relating to the incidence and distribution of colorectal carcinomas, much less is known about adenomas.The aim of our prospective study was to determine the prevalence and distribution of adenomas in a consecutive study of cases at necropsy. Over a period of approximately one year, the large bowel was examined in all cases coming to necropsy within 48 hours of death. This amounted to 365 specimens, 134 of which came from cases dying in hospital. The remaining 231 specimens were from necropsies ordered by a coroner where death had occurred outside hospital. An additional eight specimens were excluded, three where an antemortem diagnosis of large bowel cancer had been made, three where extensive autolysis precluded histological diagnosis, and two cases where the anorectal junction was not included in the specimen. MethodsAt necropsy, with the large bowel in situ, plastic clips were placed at the hepatic and splenic flexures and at the proximal and distal ends of the sigmoid colon (the point where the colon passes the inlet of the true pelvis, and the upper border of the S3 segment of the os sacrum, respectively). A portion of the terminal ileum and the whole of the large bowel, including the anorectal junction, was then removed and opened along the antimesenteric border. After washing out the contents, the total length of the bowel and its subdivisions were measured. The size, site, and configuration of any mucosal polyp was recorded on a proforma. The bowel was then pinned out flat on a cork board and immersed in a tank of 10% buffered formalin for at least 24 ho...

No abstract

The histological appearances of the liver damage occurring after a paracetamol overdose are described in liver biopsies from 104 patients, of whom 38 developed fulminant hepatic failure. Confluent centrilobular necrosis of varying extent was followed by rapid disappearance of necrotic cells, leaving areas of reticulin collapse and a usually mild inflammatory reaction. The histological recovery in even the most severe cases was remarkable, and only one of the 17 survivors whose initial biopsy showed the pattern of interlobular bridging necrosis had appreciable residual fibrosis in a follow-up biopsy taken after 1 yr. A quantitative estimate was made of the amount of surviving liver parenchyma using a morphometric technique and the hepatocyte volume fraction (HVF) in biopsies performed within 10 days of the overdose correlated well with the clinical course and both the maximal prolongation of the prothrombin time and the peak plasma bilirubin concentration in the first 10 days. An HVF value (normal 85 +/- 5 per cent.) of less than 40 per cent. in a biopsy taken within 10 days of the overdose was found only in patients who died. However, HVF measurements on biopsies from three survivors taken later than 10 days after the overdose shows that survival is possible below this critical level.

No abstract