A randomised clinical trial to assess the effect of total enteral and total parenteral nutritional support on metabolic,inflammatory and oxidative markers in patients with predicted severe acute pancreatitis (APACHEE II ≥ 6)

Background: Total enteral nutrition (TEN) within 48 h of admission has recently been shown to be safe and efficacious as part of the management of severe acute pancreatitis. Our aim was to ascertain the safety of immediate TEN in these patients and the effect of TEN on systemic inflammation, psychological state, oxidative stress, plasma glutamine levels and endotoxaemia. Methods: Patients admitted with predicted severe acute pancreatitis (APACHE II score > 5) were randomised to total enteral (TEN; n = 8) or total parenteral nutrition (TPN; n = 9). Measurements of systemic inflammation (C-reactive protein), fatigue (visual analogue scale), oxidative stress (plasma thiobarbituric acid-reactive substances), plasma glutamine and anti-endotoxin IgG and IgM antibody concentrations were made on admission and repeated on days 3 and 7 thereafter. Clinical progress was monitored using APACHE II score. Organ failure and complications were recorded. Results: All patients tolerated the feeding regime well with few nutrition-related complications. Fatigue improved in both groups but more rapidly in the TEN group. Oxidative stress was high on admission and rose by similar amounts in both groups. Plasma glutamine concentrations did not change significantly in either group. In the TPN group, 3 patients developed respiratory failure and 3 developed non-respiratory single organ failure. There were no such complications in the TEN group. Hospital stay was shorter in the TEN group [7 (4–14) vs. 10 (7–26) days; p = 0.05] as was time to passing flatus and time to opening bowels [1 (0–2) vs. 2 (1–5) days; p = 0.01]. The cost of TEN was considerably less than of TPN. Conclusion: Immediate institution of nutritional support in the form of TEN is safe in predicted severe acute pancreatitis. It is as safe and as efficacious as TPN and may be beneficial in the clinical course of this disease.     

Energy expenditure and body composition in children with Crohn's disease: effect of enteral nutrition and treatment with prednisolone

Background—Malnutrition and growth retardation arecommon complications of Crohn's disease in children. The contributionof resting energy expenditure (REE) to malnutrition is unclear.
Aims—To characterise the REE and body compositionin children with Crohn's disease and compare them with normal controlsand patients with anorexia nervosa; to compare the effects ofprednisolone and enteral nutrition on energy expenditure and body composition.
Subjects—Twenty four children with Crohn'sdisease, 19 malnourished females with anorexia nervosa, and 22 healthycontrol subjects were studied.
Methods—In children with Crohn's diseasemeasurements were done when the disease was acute and repeated at oneand three months after treatment with either prednisolone or enteralnutrition. Resting energy expenditure was measured by indirectcalorimetry and body composition by anthropometry, bioelectricalimpedance analysis, total body potassium,H₂¹⁸O, and bromide space studies.
Results—Body weight and ideal body weight weresignificantly lower in patients with Crohn's disease than in healthycontrols. Lean tissue was depleted and there was an increase inextracellular water. Per unit of lean body mass, there was nodifference between REE in patients with Crohn's disease and controls,whereas patients with anorexia nervosa had significantly reduced REE.With enteral nutrition all body compartments and REE increasedsignificantly (p<0.001). In a subgroup of age-matched men there was asignificant increase in height after three months of enteral nutritioncompared with prednisolone (p<0.01). Those treated with steroids didnot show a significant change in height but did show an increase in allbody compartments. However, intracellular water as well as lean bodymass accretion were significantly higher in the enteral nutrition groupthan in the prednisolone group.
Conclusions—Despite being malnourished, childrenwith Crohn's disease fail to adapt their REE per unit of lean bodymass. This might be a factor contributing to their malnutrition. Lean tissue accretion is higher in patients treated with enteral nutrition than in those treated with prednisolone.

Keywords:Crohn's disease; resting energy expenditure; bodycomposition; anorexia nervosa; prednisolone; enteral nutrition

     

A randomised, double blind, multicentre trial of octreotide in moderate to severe acute pancreatitis

BACKGROUND—The pharmacological inhibition of exocrine pancreatic secretion with the somatostatin analogue octreotide has been advocated as a specific treatment of acute pancreatitis.
AIM—To investigate the efficacy of octreotide in acute pancreatitis in a randomised, placebo controlled trial.
METHODS—302 patients from 32 hospitals, fulfilling the criteria for moderate to severe acute pancreatitis within 96 hours of the onset of symptoms, were randomly assigned to one of three treatment groups: group P (n=103) received placebo, while groups O1 (n=98) and O2 (n=101) received 100 and 200 µg of octreotide, respectively, by subcutaneous injection three times daily for seven days. The primary outcome variable was a score composed of mortality and 15 typical complications of acute pancreatitis.
RESULTS—The three groups were well matched with respect to pretreatment characteristics. An intent to treat analysis of all 302 patients revealed no significant differences among treatment groups with respect to mortality (P: 16%; O1: 15%; O2: 12%), the rate of newly developed complications, the duration of pain, surgical interventions, or the length of the hospital stay. A valid for efficacy analysis (251 patients) also revealed no significant differences.
CONCLUSIONS—This trial shows no benefit of octreotide in the treatment of acute pancreatitis.


Keywords: acute pancreatitis; somatostatin; octreotide; randomised controlled multicentre trial     

Total enteral nutrition vs. total parenteral nutrition in patients with severe acute pancreatitis]

OBJECTIVE: To compare the efficacy of early total enteral nutrition (TEN) vs. total parenteral nutrition (TPN) in patients with severe acute pancreatitis (SAP). METHODS: A total of 22 consecutive patients with SAP were randomized to receive TPN (group I) or TEN (group II). SAP was defined applying APACHE II score, C-reactive protein (CRP) measurements and/or Balthazar CT scan score. Acute inflammatory response (CRP, TNF-a, IL-6), visceral proteins (pre-albumin, albumin), complications (systemic inflammatory response syndrome, multiorgan failure, infections), surgical interventions, length of hospital stay and mortality were evaluated. RESULTS: No significant differences were found between the two groups in the APACHE II score, in CRP, TNF-a and IL-6 concentrations or in pre-albumin and albumin levels over the first 10 days. Seven patients in group I and 4 in group II suffered severe complications. Three patients in group I required surgical intervention. Length of hospital stay was alike in the two groups. Two patients from group I died in the course of the hospitalization. CONCLUSIONS: SAP patients with TEN feeding showed a tendency towards a better outcome than patients receiving TPN.     

Multisystemic production of interleukin 10 limits the severity of acute pancreatitis in mice

Background—Interleukin 10 (IL-10)decreases the severity of experimental acute pancreatitis. The role ofendogenous IL-10 in modulating the course of pancreatitis is currently unknown.
Aims—To examine the systemicrelease of IL-10 and its messenger RNA production in the pancreas,liver, and lungs and analyse the effects of IL-10 neutralisation incaerulein induced acute pancreatitis in mice.
Methods—Acute necrotisingpancreatitis was induced by intraperitoneal caerulein. Serum levels ofIL-10 and tumour necrosis factor (TNF), and tissue IL-10 and TNF-αgene expression were assessed. After injecting control antibody orafter blocking the activity of endogenous IL-10 by a specificmonoclonal antibody, the severity of acute pancreatitis was assessed interms of serum enzyme release, histological changes, and systemic andtissue TNF production.
Results—In control conditions,serum IL-10 levels increased and correlated with the course ofpancreatitis, with a maximal value eight hours after induction. BothIL-10 and TNF-α messengers showed a similar course, and wereidentified in the pancreas, liver, and lungs. Neutralisation ofendogenous IL-10 significantly increased the severity of pancreatitisand associated lung injury as well as serum TNF protein levels (+75%)and pancreatic, pulmonary, and hepatic TNF messenger expression (+33%,+29%, +43%, respectively).
Conclusions—In this non-lethalmodel, systemic release of IL-10 correlates with the course of acutepancreatitis. This anti-inflammatory response parallels the release ofTNF and both cytokines are produced multisystemically. Endogenous IL-10controls TNF-α production and plays a protective role in the localand systemic consequences of the disease.

Keywords:pancreatitis; interleukin 10; tumour necrosis factorα; adult respiratory distress syndrome

     

On the protective mechanisms of nitric oxide in acute pancreatitis

Background—Ectopic proteaseactivation, microcirculatory changes, and leucocyte activation are themain events in the pathogenesis of acute pancreatitis. Nitric oxide(NO) is known to be a key mediator in the normal and inflamed pancreas.
Aims—To investigate the targets onwhich NO exerts its effect in caerulein induced pancreatitis.
Methods—Acute pancreatitis wasinduced in rats which additionally received either the NO synthasesubstrate, L-arginine; the NO donor, sodium nitroprusside;or the NO synthase inhibitor, N-nitro-L-arginine methylester (L-NAME). At six hours, pancreatic injury (oedema,leucocyte content, ectopic trypsinogen activation) was analysed andpancreatic oxygenation and perfusion were determined. A directinfluence of NO on amylase secretion and trypsinogen activation wasevaluated separately in vitro.
Results—Both NO donors reduced thegrade of inflammation. L-NAME increased the severity ofinflammation, while decreasing pancreatic tissue oxygenation. Althoughneither amylase secretion nor intracellular trypsinogen activation incaerulein stimulated pancreatic acini was influenced by either NOdonors or inhibitors, both NO donors decreased intrapancreatictrypsinogen activation peptide (TAP) and pancreatic oedema in vivo, andL-NAME increased TAP.
Conclusions—NO protects againstinjury caused by pancreatitis in the intact animal but has nodiscernible effect on isolated acini. It is likely that in pancreatitisNO acts indirectly via microcirculatory changes, including inhibitionof leucocyte activation and preservation of capillary perfusion.

Keywords:acute pancreatitis; nitric oxide; microcirculation; leucocytes; pancreatic secretion

     

Total enteral nutrition as prophylactic therapy for pancreatic necrosis infection in severe acute pancreatitis.

OBJECTIVE: To evaluate the capacity of enteral nutrition, in comparison with the total parenteral nutrition (TPN) plus antibiotic therapy, for avoiding pancreatic necrosis infection in the severe acute pancreatitis. METHODS: In the period between October 1998 and September 2003, 87 patients met the inclusion criteria and took part in this research. Within the first week from their admission, 43 patients received TPN and 44 patients received total enteral nutrition (TEN). An adequate prophylactic antibiotic therapy was used in both groups. The severity of the manifestations was similar for both groups having a tomographic 'severity index' of 8 and an entry C-reactive protein of 208 and 203 mg/l, respectively. RESULTS: The group that received TPN suffered an organ failure in 79% of the cases, while the percentage showed by the group that received TEN was 31%; 88 and 25% of the patients in each group requiring a surgical intervention, respectively (p < 0.001). There was decreased presence of pancreatic necrosis infection in the group of patients that was supplied with TEN (20%) than in the group receiving TPN, where it reached 74% (p < 0.001). The death rate was significantly higher among the patients who received TPN, (35%), while for the patients who received TEN it was only 5% (p < 0.001). CONCLUSION: TEN could be used as a prophylactic therapy for infected pancreatic necrosis since it significantly diminished the necrosis infection as well as the mortality.     

The potential role of procalcitonin and interleukin 8 in the prediction of infected necrosis in acute pancreatitis

Background—Infection of pancreatic necrosis has amajor impact on clinical course, management, and outcome in acutepancreatitis. Currently, guided fine needle aspiration is the onlymeans for an early and accurate diagnosis of infected necrosis.Procalcitonin (PCT), a 116 amino acid propeptide of calcitonin, andinterleukin 8 (IL-8), a strong neutrophil activating cytokine, aremarkers of severe inflammation and sepsis.
Aims—To analyse the clinical value of PCT andIL-8 as biochemical parameters for predicting infected necrosis inacute pancreatitis.
Patients and methods—Fifty patients with acutepancreatitis entered this prospective study and were stratified intothree groups according to morphological and bacteriological findings: 18 patients with oedematous pancreatitis (group I), 14 patients withsterile necrosis (group II), and 18 patients who developed infectednecrosis a median of 13.5 days after the onset of symptoms (group III).After admission serum samples were drawn daily for two weeks.Concentrations of PCT and IL-8 were measured by chemoluminescent immunoassays (upper reference range 0.5 ng/ml for PCT and 70 pg/ml for IL-8). The routine parameter C-reactive protein was determined bylaser nephelometry (upper reference range 10 mg/l).
Results—Median concentrations of PCT and IL-8were significantly higher in patients with infected necrosis than inthose with sterile necrosis during the observation period, whereasthere was no difference in C-reactive protein. In oedematouspancreatitis overall median concentrations of all three parameters werelow. By receiver operating characteristics best cut off levels for predicting infected necrosis or persisting pancreatic sepsis were 1.8 ng/ml for PCT and 112 pg/ml for IL-8. If these cut off levels were reached on at least two days, sensitivity, specificity, and accuracy for the prediction of infected necrosis were 94%, 91%, and92% for PCT and 72%, 75%, and 74% for IL-8, respectively. Aftersurgical treatment of infected necrosis median PCT and IL-8 valuescontinued to be significantly higher in patients with persisting pancreatic sepsis (n=11) compared with those having an uneventful postoperative course (n=7). For the preoperative differentiation between infected necrosis and sterile necrosis guided fine needle aspiration was performed in 24 patients with necrotising pancreatitis and reached a diagnostic accuracy of 84% compared with 87% for PCT,and 68% for IL-8. There was no correlation between the aetiology ofacute pancreatitis or the extent of necrosis and PCT or IL-8.
Conclusion—PCT and IL-8 are found in highconcentrations in infected necrosis and associated systemiccomplications in patients with acute pancreatitis. The course of PCTshows the closest correlation with the presence of infected necrosis.Monitoring of serum PCT is a potential new marker for the non-invasiveand accurate prediction of infected necrosis as well as for theselection of patients with persisting septic complications aftersurgical debridement.

Keywords:procalcitonin; interleukin 8; infected necrosis; acute pancreatitis

     

Increased nitric oxide activity in a rat model of acute pancreatitis

Background—Overproduction of nitric oxide (NO)via induction of the inducible NO synthase (iNOS) is an importantfactor in the haemodynamic disturbances of several inflammatory states.
Aims—To identify the role of NO in a caeruleininduced model of acute pancreatitis in the rat.
Methods—Arterial blood pressure and plasma NOmetabolites were measured at zero and seven hours in adult male Wistarrats administered caerulein (n=10) or saline (n=10). Pancreaticactivity of NOS (inducible and constitutive) was assayed biochemically. The pancreatic expression and cellular localisation of NOS and nitrotyrosine (a marker of peroxynitrite induced oxidative tissue damage) were characterised immunohistochemically.
Results—Compared with controls at seven hours,the pancreatitis group displayed raised plasma NO metabolites (mean(SEM) 70.2(5.9) versus 22.7 (2.2) µmol/l, p<0.0001) and reducedmean arterial blood pressure (88.7 (4.6) versus 112.8 (4.1) mm Hg,p=0.008). There was notable iNOS activity in the pancreatitis group(3.1(0.34) versus 0.1 (0.01) pmol/mg protein/min, p<0.0001) withreduced constitutive NOS activity (0.62 (0.12) versus 0.96 (0.08)pmol/mg protein/min, p=0.031). The increased expression of iNOS wasmainly localised within vascular smooth muscle cells (p=0.003 versus controls), with positive perivascular staining for nitrotyrosine (p=0.0012 versus controls).
Conclusions—In this experimental model of acutepancreatitis, iNOS induction and oxidative tissue damage in thepancreas is associated with raised systemic NO and arterialhypotension. Excess production of NO arising from the inducible NOsynthase may be an important factor in the systemic and localhaemodynamic disturbances associated with acute pancreatitis.

     

Gut barrier function in malnourished patients

Background—The integrity of the gastrointestinalmucosa is a key element in preventing systemic absorption of enterictoxins and bacteria. In the critically ill, breakdown of gut barrier function may fuel sepsis. Malnourished patients have an increased riskof postoperative sepsis; however, the effects of malnutrition onintestinal barrier function in man are unknown.
Aims—To quantify intestinal barrier function,endotoxin exposure, and the acute phase cytokine response inmalnourished patients.
Patients—Malnourished and well nourishedhospitalised patients.
Methods—Gastrointestinal permeability wasmeasured in malnourished patients and well nourished controls using thelactulose:mannitol test. Endoscopic biopsy specimens werestained and morphological and immunohistochemical featuresgraded. The polymerase chain reaction was used to determinemucosal cytokine expression. The immunoglobulin G antibody response toendotoxin and serum interleukin 6 were measured by enzyme linkedimmunosorbent assay.
Results—There was a significant increase inintestinal permeability in the malnourished patients in associationwith phenotypic and molecular evidence of activation of lamina propriamononuclear cells and enterocytes, and a heightened acute phase response.
Conclusions—Intestinal barrier function issignificantly compromised in malnourished patients, but the clinicalsignificance is unclear.

Keywords:protein-energy malnutrition; intestinalpermeability; endotoxin; cytokine

     

Oxidative stress: an important phenomenon with pathogenetic significance in the progression of acute pancreatitis

^a Division of Gastroenterology and Intensive Care Unit, Department of Medicine, Veterans General Hospital, Taipei, and School of Medicine, National Yang-Ming University, Taiwan, ^b Department of Biochemistry, College of Medicine, National Taiwan University, Taiwan

Correspondence to: Prof. F-J Lu, Department of Biochemistry, College of Medicine, National Taiwan University, No. 1, Jen-Ai Road, Taipei, Taiwan, Republic of China.

Accepted for publication 19 January 1998

Background—Reactive oxygen species and related oxidative damage have been implicated in the initiation of acute pancreatitis. Changes in these parameters during disease progression merit further investigation.
Aims—To evaluate changes and the clinical relevance of superoxide radicals, endogenous antioxidants, and lipid peroxidation during the course of acute pancreatitis.
Patients and methods—Superoxide radicals (measured as lucigenin amplified chemiluminescence), ascorbic acid, dehydroascorbic acid, α tocopherol, and lipid peroxidation (measured as thiobarbiturate reactive substances) were analysed in blood samples from 56 healthy subjects, 30 patients with mild acute pancreatitis, and 23 patients with severe acute pancreatitis. The association with grades of disease severity was analysed. Measurements were repeated one and two weeks after onset of pancreatitis.
Results—In the blood from patients with acute pancreatitis, there were increased levels of the superoxide radical as well as lipid peroxides. There was notable depletion of ascorbic acid and an increased fraction of dehydroascorbic acid. Changes in α tocopherol were not great except in one case with poor prognosis. Differences between severe and mild acute pancreatitis were significant (p<0.01). Variable but significant correlations with disease severity scores were found for most of these markers. The normalisation of these indexes postdated clinical recovery one or two weeks after onset of disease.
Conclusions—Heightened oxidative stress appears early in the course of acute pancreatitis and lasts longer than the clinical manifestations. The dependence of disease severity on the imbalance between oxidants and natural defences suggests that oxidative stress may have a pivotal role in the progression of pancreatitis and may provide a target for treatment.
(GUT 1998;:850-855)

Keywords: acute pancreatitis;  free radicals;  superoxides;  antioxidants;  lipid peroxidation

     

Increased activity of group II phospholipase A2 in plasma in rat sodium deoxycholate induced acute pancreatitis

Background—Two different types of secretoryphospholipase A₂ (PLA₂), pancreatic group I(PLA₂-I) and non-pancreatic group II (PLA₂-II),have been identified and postulated to be associated with thepathogenesis of various diseases, such as acute pancreatitis, septicshock, and multiple organ failure.
Aims—To investigate the type of secretoryPLA₂ responsible for its catalytic activity found in plasmaand ascites of experimental acute pancreatitis.
Methods—Acute pancreatitis of differing severitywas induced by the injection of different concentrations (1% or 10%)of sodium deoxycholate (DCA) into the common biliopancreatic duct inrats, and catalytic PLA₂ activity in plasma and asciteswere differentiated by anti-PLA₂-I antibody and specificinhibitor of PLA₂-II. Survival rate and plasma amylase,aspartate aminotransferase (AST), and alanine aminotransferase (ALT)were also measured.
Results—In 1% and 10% DCA induced acutepancreatitis, plasma amylase values as well as PLA₂activity in ascites were greatly increased. PLA₂ activityin plasma was also notably increased in 10% DCA induced acutepancreatitis, but not in 1% DCA induced acute pancreatitis.PLA₂-I specific polyclonal antibody significantly inhibitedPLA₂ activity in ascites but not that in plasma. In contrast, plasma PLA₂ activity was completely suppressed byPLA₂-II specific inhibitor. In addition, a high mortality(93% at five hours) and a significant increase in plasma AST and ALTwere noted in 10% DCA induced pancreatitis.
Conclusion—Ascites PLA₂ activity ismainly derived from PLA₂-I, whereas plasma PLA₂activity is mostly derived from PLA₂-II in severe acutepancreatitis, suggesting that increased plasma PLA₂-IIactivity might be implicated in hepatic failure arising after severeacute pancreatitis.

Keywords:acute pancreatitis; phospholipase A₂; sodium deoxycholate pancreatitis; hepatic failure

     

Inhibition of nuclear factor-κB activation improves the survival of rats with taurocholate pancreatitis

Background—Death inthe early stages of severe acute pancreatitis is frequently the resultof multiple organ dysfunction, but its mechanism is not clear.
Aims—To investigatethe state of nuclear factor-κB (NF-κB) in macrophages of rats withlethal pancreatitis, and to assess the effectiveness of pyrrolidinedithiocarbamate, an inhibitor of NF-κB, on the pathology and mortality.
Methods—Taurocholatepancreatitis was produced in rats, and the severity of the disease, themortality, and activation of NF-κB in peritoneal and alveolarmacrophages were compared in rats receiving pyrrolidine dithiocarbamate(PDTC) treatment and those that were not.
Results—Taurocholatepancreatitis produced massive necrosis, haemorrhage, and severeleucocyte infiltration in the pancreas as well as alveolar septalthickening in the lung. NF-κB was activated in peritoneal andalveolar macrophages six hours after pancreatitis induction.Pretreatment with PDTC dose-dependently attenuated the NF-κBactivation and improved the survival of the rats, although it did notaffect the early increase in serum amylase and histological findings.
Conclusions—Earlyblockage of NF-κB activation may be effective in reducing fataloutcome in severe acute pancreatitis.

Keywords:pancreatitis; multiple organ dysfunction; nuclearfactor-κB; pyrrolidine dithiocarbamate; macrophages; rat

     

Nutritional support in acute pancreatitis: an update on management issues

About 20% of acute pancreatitis cases develop necrosis and have a high risk of inflammatory and infectious complications and a high mortality rate. Acute pancreatitis has a variety of causes and despite years of research its pathogenesis remains complex and obscure. Both local and systemic inflammatory responses play key roles in the pathophysiology of this disorder. Treatment plans continue to rely on supportive care without proven specific therapies. Pancreatic rest and use of total parenteral nutrition (TPN) were the gold standard for nutritional support of these challenging patients. Because numerous studies in other critically ill patients demonstrated benefits of enteral nutrition, recent investigations compared TPN to enteral nutrition in acute pancreatitis. These studies indicated that enteral nutrition delivered into the jejunum was tolerated well, even in patients with severe acute pancreatitis. "Mild' cases of pancreatitis should improve and tolerate oral nutrition within a few days. In contrast, "severe' cases of pancreatitis or those with a protracted clinical course require nutritional support to aid in preventing adverse effects of starvation and nutrient deficiencies. Current recommendations are to attempt enteral nutrition in patients with acute pancreatitis prior to instituting TPN. Further studies to determine optimal nutrient composition are warranted and should investigate the possibility of modulating the inflammatory response induced by pancreatitis to improve outcomes.     

Lesion characteristics of acute myocardial infarction: an investigation with intravascular ultrasound

OBJECTIVE—To use intravascular ultrasound (IVUS) to compare plaque morphology in acute myocardial infarction and stable angina pectoris.
DESIGN—Retrospective study.
SETTING—Primary care hospital.
PATIENTS—59 consecutive cases of acute myocardial infarction and 50 consecutive cases of stable angina pectoris.
METHODS—IVUS was used before coronary intervention.
MAIN OUTCOME MEASURES—Plaque morphology (incidence of eccentric plaque, subtle dissections, low echoic thrombus, calcification, echolucent areas, and bright speckled echo material), assessed visually using IVUS.
RESULTS—There were no significant differences in plaque eccentricity or calcification between the two groups, but low echoic thrombus (acute myocardial infarction 15% v stable angina pectoris 0%), subtle dissections (37% v 4%), echolucent areas (31% v 0%), and bright speckled echo material (90% v 0%) were more common in the infarction group than in the stable angina group (p < 0.001 for all). There was a longer time between the onset of symptoms and the IVUS examination in patients with low echoic thrombus than in those without (p < 0.03).
CONCLUSIONS—Low echoic thrombus, subtle dissections, echolucent areas, and bright speckled echo material are morphological characteristics associated with plaque at the time of acute myocardial infarction. These findings correspond pathologically to ruptured plaque.


Keywords: intravascular ultrasound; acute myocardial infarction; plaque morphology     

Non-alcoholic duct destructive chronic pancreatitis

Background—The pathology of non-alcoholic chronicpancreatitis has not yet been sufficiently studied.
Aims—To identify the major changes of pancreatictissue in patients surgically treated for non-alcoholic chronic pancreatitis.
Patients—Pancreatectomy specimens from12 patients with non-alcoholic chronic pancreatitis, including fourpatients with autoimmune or related diseases (Sjögren's syndrome,primary sclerosing cholangitis, ulcerative colitis, and Crohn'sdisease), were reviewed.
Methods—Morphological changes were studiedhistologically and immunohistochemically (to type inflammatory cells)and compared with the pancreatic alterations found in 12 patients withalcoholic chronic pancreatitis.
Results—In patients with non-alcoholic chronicpancreatitis, with or without associated autoimmune or relateddiseases, pancreatic inflammation particularly involved the ducts,commonly resulting in duct obstruction and occasionally ductdestruction. None of these features was seen in alcoholic chronicpancreatitis which, however, showed pseudocysts and calcifications.
Conclusion—The pancreatic changes in patients withnon-alcoholic chronic pancreatitis clearly differ from those withalcoholic chronic pancreatitis. The term chronic duct destructivepancreatitis is suggested for this type of pancreatic disease.

     

The role of extra-pancreatic infections in the prediction of severity and local complications in acute pancreatitis

Background

The aim of our study was to determine the risk factors for extrapancreatic infection (EPI) occurrence and its predictive power for assessing severity and local complications in acute pancreatitis including infected pancreatic necrosis (IPN).

Plaque erosion is a major substrate for coronary thrombosis in acute myocardial infarction

OBJECTIVE—To evaluate the prevalence of plaque erosion as a substrate for coronary thrombosis.
DESIGN—Pathological study in patients with acute myocardial infarction not treated with thrombolysis or coronary interventional procedures.
PATIENTS—298 consecutive patients (189 men, mean (SD) age 66 (11) years; 109 women, 74 (8) years) dying in hospital between 1984 and 1996 from acute myocardial infarction, diagnosed by ECG changes and rise in cardiac enzymes.
MAIN OUTCOME MEASURES—Histopathological determination of plaque erosion as substrate for acute thrombosis; location and histological type of coronary thrombosis; acute and healed myocardial infarcts; ventricular rupture.
RESULTS—Acute coronary thrombi were found in 291 hearts (98%); in 74 cases (25%; 40/107 women (37.4%) and 34/184 men (18.5%); p = 0.0004), the plaque substrate for thrombosis was erosion. Healed infarcts were found in 37.5% of men v 22% of women (p = 0.01). Heart rupture was more common in women than in men (22% v 10.5%, p = 0.01). The distribution of infarcts, thrombus location, heart rupture, and healed infarcts was similar in cases of plaque rupture and plaque erosion.
CONCLUSIONS—Plaque erosion is an important substrate for coronary thrombosis in patients dying of acute myocardial infarction. Its prevalence is significantly higher in women than in men.


Keywords: plaque erosion; rupture; acute myocardial infarction     

A new performance indicator for acute myocardial infarction

OBJECTIVE—To develop a performance indicator for acute myocardial infarction which would reliably measure success of treatment and which might provide an alternative to case fatality as an audited outcome.
DESIGN—A two year audit of all cases of acute myocardial infarction and resuscitated cases of out of hospital cardiac arrest from coronary heart disease in patients under 75 years of age. Behaviour of patients in calling for help, performance of the ambulance services in treating out of hospital arrest, and of the hospitals in providing resuscitation and thrombolytic treatment are audited separately.
SETTING—Four district general hospitals.
AUDITED INTERVENTIONS—Resuscitation from cardiac arrest and thrombolytic treatment.
MAIN OUTCOME MEASURES—Hospital case fatality and lives saved/1000 patients treated.
RESULTS—Overall, the lives of 83/1000 patients were saved (95% confidence interval 70 to 96). Of these, 29 (35%) were saved by out of hospital resuscitation and 38 (46%) by in hospital resuscitation from cardiac arrest. It was estimated that 16 lives (19%) were saved by thrombolytic treatment. There were no significant differences in case fatality among the hospitals.
CONCLUSIONS—Lives saved/1000 patients treated is an easily measurable index and assesses performance of the ambulance service as well as of the hospital. Because it is relatively insensitive to diagnostic definitions, it may provide a robust alternative to case fatality as a performance indicator.


Keywords: acute myocardial infarction; audit; case fatality; outcome indicators     

Prognostic implications of ventricular fibrillation in acute myocardial infarction: new strategies required for further mortality reduction

OBJECTIVE—To determine the changing risk of ventricular fibrillation, the prognostic implications, and the potential long term prognostic benefit of earlier hospital admission, after acute myocardial infarction.
DESIGN—Prospective observational study.
SETTING—A district general hospital in east London.
PATIENTS—1225 consecutive patients admitted to a coronary care unit with acute myocardial infarction.
MAIN OUTCOME MEASURES—Time of onset of pain and ventricular fibrillation, and long term survival of patients admitted with acute myocardial infarction.
RESULTS—The rate of ventricular fibrillation in these hospital inpatients was high in the first hour from onset of pain (118 events/1000 persons/h; 95% confidence interval (CI) 50.7 to 231) and fell rapidly to an almost constant low level by six hours; 27.4% of patients with early ventricular fibrillation died in hospital, compared with 11.6% of those without (p < 0.0001), but mortality in patients who survived to hospital discharge was not altered by early ventricular fibrillation (five year survival: 75.0% (95% CI 60.0% to 84.8%) with ventricular fibrillation v 73.3% (95% CI 69.6% to 76.6%) without ventricular fibrillation).
CONCLUSIONS—Patients successfully resuscitated from early ventricular fibrillation have the same prognosis as those without ventricular fibrillation after acute myocardial infarction. Faster access to facilities for resuscitation must be achieved if major improvements in the persistently high case fatality of patients after acute myocardial infarction are to be made.


Keywords: ventricular fibrillation; acute myocardial infarction; prognosis