A prospective audit of acute pancreatitis involving nine hospitals in the North-West Thames Region recruited 631 patients over 54 months. There were 57 deaths (9 per cent); a diagnosis had been reached in 50 patients (88 per cent) before death and in seven (12 per cent) at autopsy. Eighteen patients (32 per cent) died within the first week, usually as a result of multisystem organ failure (15 patients). Thirty-nine patients (68 per cent) died after the first week from complications related to infection (26 patients) co-morbid conditions (nine) or non-infective complications (four). Twenty-one patients (42 per cent) had been inadequately evaluated by Ranson's criteria, and only 22 (44 per cent) of 50 with a premortem diagnosis of pancreatitis had undergone computed tomography (CT). Fifteen of 26 patients who died from infection-related complications had CT and only nine underwent necrosectomy or surgical drainage. These data suggest that improved diagnosis, investigation and management of patients with acute pancreatitis is possible, and may result in improved clinical outcome.

Recovery of liver cell mass following hepatectomy requires a metabolic compromise between differentiated function and organ regrowth. Clinical experience has shown that hepatic failure after resection is more common when the organ is diseased. We have evaluated intracellular hepatic biochemistry in patients with normal and cirrhotic livers undergoing partial hepatectomy, using 31-phosphorus magnetic resonance spectroscopy ( 31 P MRS). Eighteen patients were studied, half with normal liver architecture (normal group, n ‫؍‬ 9) and half with cirrhotic parenchyma (cirrhosis group, n ‫؍‬ 9). Magnetic resonance examinations were performed preoperatively and on postoperative days 2, 4, 6, 14, and 28. Hepatic volume (estimated by magnetic resonance imaging [MRI]) and blood chemistries were measured at the same intervals. Following a comparable reduction in parenchymal volume, the cirrhotic group demonstrated a more sustained fall in adenosine triphosphate (ATP) energy state. Disturbance of membrane phospholipid metabolism and duration of acute-phase reaction were more marked when the liver was diseased. The pattern of derangement of hepatic function, however, was similar in the two groups. Overall, the recovery process was less efficient in the cirrhotic organ, and culminated in a diminished rate and extent of the regenerative response. These outcomes indicate that liver regeneration after partial hepatectomy involves modulation of hepatic energy economy in response to changing work demands. The efficiency of this process is influenced by the histopathologic state of the organ, and in turn governs the physiologic reserve. These findings may explain the mechanism of posthepatectomy liver failure, and offer a rational basis for the assessment of novel hepatic support strategies. (HEPATOLOGY 2001;34:557-565.)The liver has a remarkable ability to replace lost cell mass. This capacity for regeneration is exploited clinically when partial hepatectomy is used in the treatment of disease. After liver resection, the remaining hepatocytes must reach a metabolic compromise between sustained differentiated function and cellular proliferation. 1 These competing demands for energy should be matched by compensatory changes in adenosine triphosphate (ATP) availability if energy balance and organ performance are to be maintained. Clinical experience has shown that recovery after liver resection is related to the histopathologic condition of the parenchyma, the risk of hepatic failure being higher when cirrhosis is present. 2 Traditionally, the clinical assessment of liver function during regeneration has relied on indirect measurement based on blood proteins and plasma biochemical indices. Extensively studied in classical animal models, our knowledge of the cellular processes that underlie these events in humans is incomplete, largely because of the unfeasible requirement for serial biopsy specimens. 3 We have used image-guided in vivo 31-phosphorus magnetic resonance spectroscopy ( 31 P MRS) to assess the hepatic biochemical response i...

No abstract

ObjectiveTo elucidate the metabolic changes occurring within hepatocytes during acute phase reaction and liver regeneration. Summary Background DataThe metabolic events occurring within the liver during the hepatic stress response are poorly understood. The authors used in vivo 31-phosphorus magnetic resonance spectroscopy to study hepatic metabolism after surgical trauma with and without loss of liver cell mass. MethodsThree groups were studied: five patients undergoing partial hepatectomy; five patients in whom laparotomy and colonic resection was performed; and five patients treated by thyroidectomy. Hepatic metabolism was evaluated by 31-phosphorus magnetic resonance spectroscopy before surgery and serially thereafter on postoperative days 2, 4, 6, 14, and 28. Estimation of liver volume by magnetic resonance imaging and blood sampling for biochemistry were performed at the same time points. ResultsThe authors found that alterations in hepatocyte phospholipid metabolism occurred after surgery that were correlated with changes in circulating acute phase proteins. Liver regeneration after hepatectomy was also associated with a derangement in energy metabolism, measured by a decrease in the ratio of ATP to its hydrolysis product inorganic phosphate. The depleted energy status was mirrored in biochemical indices of liver function, and restitution paralleled the course of restoration of hepatic cell mass. ConclusionsThese findings indicate that changes in liver metabolism after surgery reflect the magnitude of tissue injury and the quantity of functioning liver cells. Acute phase responses dominate the initial recovery period at the expense of less important endergonic functions. When liver parenchyma is lost, the acute phase reaction is maintained and further supported by a rapid replenishment of hepatocytes, which can even be considered a continuation of acute phase physiology. Modulation of liver function within the framework of overall hepatic energy economy is one mechanism for matching energy supply with increased demands during these processes.The liver plays a central role in the coordinated metabolic response to injury. Somatic tissue damage is associated with an acute phase reaction at the hepatocyte level characterized by a major redirection of protein synthesis, designed to restore bodily homeostasis.1 This response is maintained even after a sudden reduction in the number of hepatocytes induced by injury or surgery, when it is supplanted by a rapid compensatory replenishment of lost liver cells.2 The mechanisms of metabolic control and maintenance of liver function during these dynamic events are incompletely understood. Traditionally, the assessment of liver function has relied on indirect measurement based on circulating blood proteins and biochemical indices. We have applied the technology of image-guided in vivo 31-phosphorus mag-