American Journal of Gastroenterology ISSN0002-9270 C 2006by Am.Coll.of Gastroenterology doi:10.1111/j.1572-0241.2006.00856.x Published by Blackwell Publishing
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Practice Guidelines in Acute Pancreatitis
Peter A.Banks,M.D.,M.A.C.G.,1Martin L.Freeman,M.D.,F.A.C.G.,2and the Practice Parameters Committee of the American College of Gastroenterology∗
1Division of Gastroenterology,Center for Pancreatic Dia,Brigham and W omen’s Hospital,Harvard Medical School,Boston,Massachutts;2Division of Gastroenterology,Hennepin County Medical Center, University of Minnesota,Minneapolis,Minnesota
(Am J Gastroenterol2006;101:2379–2400)
INTRODUCTION
Guidelines for the diagnosis and treatment of acute pancre-atitis were published by the American College of Gastroen-terology in1997(1).The and subquent guidelines(2–7) have undergone periodic review(6,8–13)in accordance with advances that have been made in the diagnosis and treatment of acute pancreatitis.Guidelines for clinical practice are in-tended to apply to all health-care p
roviders who take care of patients with acute pancreatitis and are intended to beflexi-ble,and to suggest preferable(but not the only)approaches. Becau there is a wide range of choices in any health-care situation,the physician should lect the cour best suited to the individual patient and the clinical situation.
The guidelines have been developed under the auspices of the American College of Gastroenterology and its Prac-tice Parameters Committee,and approved by the Board of Trustees.The world literature in English was reviewed us-ing a MEDLINE arch and also using the Cochrane Library. The ratings of levels of evidence for the guidelines are indi-cated in Table1.Thefinal recommendations are bad on the data available at the time of the publication of this document and may be updated with appropriate scientific development at a later time.The following guidelines are intended for adult and not pediatric patients.The main diagnostic guide-lines include an asssment of risk factors of verity at ad-mission and determination of verity.The major treatment guidelines include supportive care,fluid resuscitation,trans-fer to intensive care unit,enteral feeding,u of antibiotics, treatment of infected pancreatic necrosis,treatment of sterile pancreatic necrosis,treatment of associated pancreatic duct disruptions,and role of magnetic resonance cholangiopan-creatography(MRCP),endoscopic ultrasound(EUS),and en-doscopic retrogr
ade cholangiopancreatography(ERCP)with biliary sphincterotomy for detection and treatment of chole-docholithiasis in biliary pancreatitis.
∗The members of the Practice Parameters Committee of the American College of Gastroenterology are listed in the Appendix.PATHOPHYSIOLOGY
The pathophysiology of acute pancreatitis is generally consid-ered in three phas.In thefirst pha,there is premature ac-tivation of trypsin within pancreatic acinar cells.A variety of mechanisms have been propod including disruption of cal-cium signaling in acinar cells(14–18),cleavage of trypsino-gen to trypsin by the lysosomal hydrola cathepsin-B,and decread activity of the intracellular pancreatic trypsin in-hibitor(17,18).Once trypsin is activated,it activates a variety of injurious pancreatic digestive enzymes.
In the cond pha,there is intrapancreatic inflammation through a variety of mechanisms and pathways(16,18–28). In the third pha,there is extrapancreatic inflammation in-cluding acute respiratory syndrome(ARDS)(16,19–21,29). In both phas,there are four important steps mediated by cytokines and other inflammatory mediators:1)activation of inflammatory cells,2)chemoattraction of activated inflam-matory cells to the microcirculation,3)activation of adhe-sion molecules allowing t
he binding of inflammatory cells to the endothelium,and4)migration of activated inflammatory cells into areas of inflammation.
In the majority of patients,acute pancreatitis is mild.In10–20%,the various pathways that contribute to incread intra-pancreatic and extrapancreatic inflammation result in what is generally termed systemic inflammatory respon syndrome (SIRS)(Table2).In some instances,SIRS predispos to multiple organ dysfunction and/or pancreatic necrosis.The factors that determine verity are not clearly understood,but appear to involve a balance between proinflammatory and anti-inflammatory factors.Recent evidence suggests that the balance may be tipped in favor of proinflammatory factors by genetic polymorphisms of inflammatory mediators that increa verity of acute pancreatitis(27,30,31). CLINICAL CONSIDERATIONS
Clinical Diagnosis
It has been estimated that in the United States there are 210,000admissions for acute pancreatitis each year(13). Most patients with acute pancreatitis experience abdominal
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2380Banks et al.
Table1.Ratings of Evidence Ud for This Guideline
I.Strong evidence from at least one published systematic review of multiple well-designed randomized controlled trials
II.Strong evidence from at least one published properly designed randomized controlled trial of appropriate size and in an appropriate clinical tting
III.Evidence from published well-designed trials without randomization,single group prepost,cohort,time ries,or matched ca-controlled studies
IV.Evidence from well-designed nonexperimental studies from more than one center or rearch group or opinion of respected authorities,bad on clinical evidence,descriptive studies,or reports of expert connsus committees
职场英语网pain that is located generally in the epigastrium and radiates to the back in approximately half of cas.The ont may be swift with pain reaching maximum intensity within30min, is frequently unbearable,and characteristically persists for more than24h without relief.The pain is often associated with naua and vomiting.Physical examination usually re-veals vere upper abdominal tenderness at times associated with guarding(32).
There is general acceptance that a diagnosis of acute pan-creatitis requires two of the following three features:1)ab-dominal pain characteristic of acute pancreatitis,2)rum amyla and/or lipa≥3times the upper limit of normal, and3)characteristicfindings of acute pancreatitis on CT scan.This definition allows for the possibility that an amyla and/or lipa might be<3times the upper limit of normal in acute pancreatitis.In a patient with abdominal pain charac-teristic of acute pancreatitis and rum enzyme levels that are lower than3times the upper limit of normal,a CT scan must be performed to confirm a diagnosis of acute pancreatitis.In addition,this definition allows for the possibility that pres-ence of abdominal pain cannot be assd in some patients with verely altered mental status due to acute or chronic illness.
In general,both amyla and lipa are elevated during the cour of acute pancreatitis.The rum lipa may re-main elevated slightly longer than amyla.The height of the rum amyla and/or lipa does not correlate with the verity of acute pancreatitis.It is usually not necessary to measure both rum amyla and lipa.Serum lipa may be preferable becau it remains normal in some nonpancreatic conditions that increa rum amyla including macroamy-lamia,parotitis,and some carcinomas.In general,rum lipa is thought to be more nsitive and specific than rum amyla in the diagnosis of acute pancreatitis.Daily mea-Table2.Systemic Inflammatory Respon Syndrome(SIRS)
Defined by Two or More of the Following Criteria:
Pul>90beats/min
Respiratory rate>20/min or PCO2<32mmHg
Rectal temperature<36◦C or>38◦C
White blood count<4,000or>12,000/mm3surement of rum amyla or lipa after the diagnosis of acute pancreatitis has limited value in asssing the clinical progress of the illness or ultimate prognosis(32).If rum amyla and/or lipa remain elevated for veral weeks,pos-sibilities include persisting pancreatic/peripancreatic inflam-mation,blockage of the pancreatic duct,or development of a pudocyst.
什么是bbsThe differential diagnosis of acute pancreatitis is broad and includes menteric ischemia or infarction,perforated gastric or duodenal ulcer,biliary colic,discting aortic aneurysm, intestinal obstruction,and possibly inferior wall myocardial infarction.In vere pancreatitis,the patients appear toxic and quite ill.In mild pancreatitis,the patients generally appear uncomfortable but not as ill(32).
A detailed discussion of the approach to determining the etiology of acute pancreatitis is beyond the
scope of this pa-per.During the initial hospitalization for acute pancreatitis, reasonable attempts to determine etiology are appropriate, and in particular tho caus that may affect acute manage-ment.Relevant historical clues include any previous diag-nosis of biliary tract dia or gallstones,cholecystectomy, other biliary or pancreatic surgery,acute or chronic pancre-atitis or their complications,u of ethanol,medications and the timing of their initiation,recent abdominal trauma,weight loss or other symptoms suggesting a malignancy,or a family history of pancreatitis.Blood tests within thefirst24h should include liver chemistries,calcium,and triglycerides. Abdominal ultrasound is usually performed at the time of admission to asss for gallstones as the etiology rather than to establish the diagnosis of acute pancreatitis.Detec-tion of common bile duct stones by ultrasound is limited by poor nsitivity,although specificity is quite high if they are identified.Dilation of the common bile duct alone is neither nsitive nor specific for the detection of common bile duct stones.Occasionally,the pancreas is well enough en by ab-dominal ultrasound to reveal features that are consistent with the diagnosis of acute pancreatitis including diffu glandular enlargement,hypoechoic texture of the pancreas reflective of edema,and ascites.Contrast-enhanced CT scan(and in par-ticular a contrast-enhanced thin-ction multidetector-row CT scan)is the best imaging technique to exclude conditions that masquerade as acute pancreatitis,to diagno the verity of acute pancreatitis,and to identify complications of pancre-atitis(33–35).Findings on CT
scan that confirm the diagno-sis of acute pancreatitis include enlargement of the pancreas with diffu edema,heterogeneity of pancreatic parenchyma, peripancreatic stranding,and peripancreaticfluid collections. With the u of IV contrast,a diagnosis of pancreatic necrosis can be established.In addition,contrast-enhanced CT scan may give clues as to the etiology of acute pancreatitis:for ex-ample,a common bile duct stone may occasionally be directly visualized,pancreatic calcifications may indicate underlying chronic pancreatitis due to alcohol or other caus,a pan-creatic mass may suggest malignancy,and diffu dilation of the pancreatic duct or a cystic lesion may suggest intra-ductal papillary mucinous neoplasia or cystic neoplasm.The
Practice Guidelines in Acute Pancreatitis2381
Table3.Severe Acute Pancreatitis as Defined by Atlanta Sympo-sium
Early Prognostic Signs
中国研究生网上报名Ranson signs≥3
APACHE-II score≥8
Organ Failure
and/or
Local Complications
Necrosis
Abscess
Pudocyst
role of magnetic resonance imaging(MRI)and MRCP in the diagnosis of acute pancreatitis and establishment of verity is undergoing evaluation.The techniques are superior to CT scan in delineating pancreatic ductal anatomy(36–38) and detecting choledocholithiasis(39).
Definitions
The International Symposium,held in Atlanta,GA,in1992, established a clinically bad classification system for acute pancreatitis(40,41).The goal was to establish international standards of definitions of acute pancreatitis and its compli-cations to make possible valid comparisons of verity of illness and results of therapy and also to establish criteria for patient lection in randomized prospective tri
als.Accord-ing to the Atlanta Symposium,acute pancreatitis was defined as an acute inflammatory process of the pancreas that may also involve peripancreatic tissues and/or remote organ sys-tems.Criteria for verity included organ failure(particularly shock,pulmonary insufficiency,and renal failure)and/or lo-cal complications(especially pancreatic necrosis but also in-cluding abscess and pudocyst).Early predictors of verity within48h of initial hospitalization included Ranson signs and APACHE-II points(Table3).
Interstitial pancreatitis was defined as focal or diffu enlargement of the pancreas with enhancement of the parenchyma that is either homogeneous or slightly heteroge-neous in respon to IV contrast.There may be inflammatory changes in peripancreatic fatty tissue characterized by a hazy appearance.
Pancreatic necrosis was defined as diffu or focal ar-eas of nonviable pancreatic parenchyma that was typically associated with peripancreatic fat necrosis.The criteria for the CT diagnosis of necrosis included focal or diffu well-marginated zones of nonenhanced pancreatic parenchyma greater than3cm in size or greater than30%of the pan-creas.It was recognized that pancreatic necrosis could be either sterile or infected and that infected necrosis was char-acterized by the prence of bacteria(and/or fungi)within the necrotic tissue.
An extrapancreaticfluid collection was defined as pancre-aticfluid that extravasates out of the pancreas during acute pancreatitis into the anterior pararenal spaces and other areas as well.Fluid collections may occur both with interstitial and Table4.Organ Failure as Defined by Atlanta Symposium
Shock–systolic pressure<90mmHg
PaO2≤60mmHg
Creatinine>2.0mg/L after rehydration
Gastrointestinal bleeding>500cc/24h
necrotizing pancreatitis.Mostfluid collections remain sterile and disappear during the recovery period.
A pancreatic pudocyst was defined as a collection of pancreatic juice enclod by a nonepithelialized wall that oc-curs as a result of acute pancreatitis,pancreatic trauma,or chronic pancreatitis.It is generally believed that a period of at least4wk is required from the ont of acute pancre-atitis to form a well-defined wall compod of granulation andfibrous tissue.Pancreatic pudocysts contain consider-able pancreatic enzymes and are usually sterile.According to the Atlan
ta Symposium,an infected pancreatic pudocyst should be termed a pancreatic abscess.A pancreatic abscess may also occur when an area of pancreatic necrosis undergoes condary liquefaction and then becomes infected.
Mild acute pancreatitis was defined as pancreatitis asso-ciated with minimal organ dysfunction and an uneventful recovery.Severe pancreatitis was defined as pancreatitis as-sociated with organ failure and/or local complications(necro-sis,abscess,or pudocyst).
Organ failure was defined as shock,pulmonary insuffi-ciency,renal failure,or gastrointestinal bleeding(Table4). There were a number of additional systemic complications that were identified as characteristic of vere acute pan-creatitis including disminated intravascular coagulation (platelets≤100,000/mm3,fibrinogen≤100mg/dL,fibrin split products>80μg/mL),or a vere metabolic disturbance (rum calcium≤7.5mg/dL).
The Atlanta Symposium was an important initiative in es-tablishing a clinically bad classification system.However, it is now clear some of the information included in the classi-fication was subject to different interpretations,and that crite-ria of verity as defined by the Atlanta Symposium have not been ud in a uniform fashion in recent publications(3,10, 13,25,27,31,42–165).In addition,there is
new scientific in-formation that should be included in a revid classification. Areas of major concern are as follows:
1.In the Atlanta Symposium,a uniform threshold was not
established for rum amyla and/or lipa for the diag-nosis of acute pancreatitis.In recently published articles, the threshold varied from≥2times to≥4times the upper limit of normal.
2.In the Atlanta Symposium,criteria for vere pancre-
atitis included organ failure and/or local complications (Table3).This broad definition describes a heterogeneous group of patients with varying levels of verity.For exam-ple,the prognosis of pancreatic necrosis is more rious than a pudocyst or pancreatic abscess.Also,almost all patients with necrotizing pancreatitis without organ fail-ure survive,whereas tho with multisystem organ failure
2382Banks et al.ui设计学校
Table5.Mortality in Acute Pancreatitis
Median(%)Range(%)References
All cas52–92,25,44,46,50,56,59,61,73,75,76,86,109,140,168 Interstitial pancreatitis31–746,50,82,133,145,153,168
Necrotizing pancreatitis178–3946,50,54,55,59,60,66,67,75,83,86,91,92,109,111,113,
114,120,121,128,133,145,147,148,153,168,169
Infected necrosis3014–6245,62–64,68,69,83,109–111,113,118,120,121,126,128,
134,138,148,161,164,170
Sterile necrosis122–4468,83,109–111,113,118,120,121,128,134,138,148,161,170
have a median mortality of47%(48,66,68,83,120,163, 164).
3.There was no distinction between transient and persistent
organ failure.Patients with persistent organ failure have
a more rious prognosis than tho with transient organ
failure(71,72,151).
4.Criteria for organ failure that were established have not
been ud in a uniform fashion.Some reports have re-stricted organ failure to shock,hypotension,renal failure, and gastrointestinal bleeding(10,13,44,46,50–52,57, 73,74,83,84,89,140,145,148).Other reports have altered thresholds for organ failure,or have included ad-ditional criteria,or have ud alternative or nonspecified scoring systems(3,25,31,43,45,47,48,53,54,56,58–61,64,66–69,77–80,82,86–88,90–95,97–100,102, 103,105–112,114,119–123,125–129,134–136,138, 139,142,143,146,147,149–153,155,156,159–161, 165).A revision of the Atlanta criteria will undoubtedly delete gastrointestinal bleeding(which is rarely encoun-tered in acute pancreatitis)and will retain shock,hypoten-sion,and renal failure as the important components of or-gan failure.In addition,a revision will likely include one of the formal scoring systems for organ failure that are currently available.
5.In the Atlanta Symposium,pancreatic necrosis was con-
sidered as either greater than30%of the pancreas or greater than3cm in size.The are,in effect,two differ-ent definitions.Becau of the variability in the minimum criteria ud for the prence of necrosis,it is difficult to compare studies from different institutions(10,13,25,27, 31,44–60,62–64,66–
74,77–92,98,100–102,104–107, 113,115,116,119–121,126–129,131,133–135,137, 138,140,142–148,150,153,154,156,157,159,161).
A revision of the Atlanta criteria will undoubtedly pro-
vide a uniform threshold for the diagnosis of pancreatic necrosis.
6.Regarding the term pancreatic pudocyst,a distinction
was not made between two relatively distinctive entities.
Thefirst is a collection of pancreatic juice enclod by
a nonepithelialized wall that occurs mostly near the pan-
creas.While the contents may also include peripancreatic necrotic material,the contents are usually mostlyfluid.
The cond type of pancreatic pudocyst is that which takes place within the confines of the pancreas and in-volves pancreatic necrotic tissue with variable amounts
of pancreaticfluid.This entity,frequently termed“orga-nized necrosis”(166),is a distinct clinical entity that pos substantially greater management challenges(167).Ad-ditional terminology will be needed to parate the two conditions.
Overview of Acute Pancreatitis
Overall,85%of patients have interstitial pancreatitis;15% (range4–47%)have necrotizing pancreatitis(25,44,46,50, 68,83,86,128,140,169).Among patients with necrotizing pancreatitis,33%(range16–47%)have infected necrosis(62, 66,68,83,91,111,113,117,118,120,121,147,159,169, 170).
Approximately10%of patients with interstitial pancreati-tis experience organ failure,but in the majority it is transient with a very low mortality.Median prevalence of organ failure in necrotizing pancreatitis is54%(range29–78%)(31,50, 54,82,83,120,147,148).Prevalence of organ failure is the same or somewhat higher in infected necrosis(34–89%)than in sterile necrosis(45–73%)(66,83,138,161).
The overall mortality in acute pancreatitis is approximately 5%:3%in interstitial pancreatitis,17%in necrotizing pan-creatitis(30%in infected necrosis,12%in sterile necrosis) (Table5).
The mortality in the abnce of organ failure is0(50,66, 68,83),with single organ failure is3%(range0–8%)(66,83, 163),with multisystem organ failure47%(range28–69%) (48,66,68,83,120,163,164).
Although older literature suggested that80%of deaths oc-cur after veral weeks of illness as a result of infected necro-sis,more recent surveys have shown considerable variation with veral reports showing a reasonably even distribution of early deaths(within1–2wk)versus later deaths(46,72,76, 150,151,163),a few showing the majority of deaths within thefirst2wk(67,75),and others showing the majority of deaths after thefirst2wk(59,89,135).The variations re-flect a variety of influences including percentage of very ill patients referred to a reporting hospital compared to patients admitted directly.Deaths within thefirst2wk are generally attributed to organ failure;deaths after this interval are gen-erally caud by infected necrosis or complications of sterile necrosis.
Practice Guidelines in Acute Pancreatitis2383
DIAGNOSTIC GUIDELINE I:LOOK FOR RISK FACTORS OF
SEVERITY AT ADMISSION
Older age(>55),obesity(BMI>30),organ failure at admis-
sion,and pleural effusion and/or infiltrates are risk factors for
verity that should be noted at admission.Patients with the
characteristics may require treatment in a highly supervid
area,such as a step-down unit or an intensive care unit.
Level of evidence:III
The importance of establishing risk factors of verity of
acute pancreatitis at admission is veral-fold:to transfer
tho patients who are most likely to have a vere episode
to a step-down unit or an intensive care unit for clor su-
pervision,to allow physicians to compare results of optimal
therapy,and to facilitate the identification of riously ill pa-
tients for inclusion in randomized prospective trials.A variety
of potential risk factors have been investigated as follows.
It is intuitive that older individuals would have more vere
大学英语四级作文范文pancreatitis becau of comorbid dia.In many(50,55,
60,67,70,75,83,86–88,91,128)but not all(31,46,53,
61,165,168)reports,older age(generally≥55yr of age)has
correlated with a more vere prognosis.
There have been a variety of studies that have sought to
determine whether obesity is a risk factor for verity in
acute pancreatitis(56–60,75,87,88).A recent meta-analysis
concluded that obe patients(defined as tho with a BMI >30)had more systemic and local complications but not greater mortality(57).In one recent report,the combination
of AP ACHE-II and obesity(a classification termed AP ACHE-
O)measured within thefirst24h of admission improved the
prediction of verity in patients with acute pancreatitis(58).
Several reports have pointed out that patients with organ词组翻译
failure at admission have a higher mortality than tho who
do not experience organ failure at admission(50,61,69,
71,72,83,163).The progression of single organ failure to
multisystem organ failure is a major determinant in the high
mortality associated with organ failure at admission(83).
华东师范大学第二附属中学Survival among patients with organ failure at admission has
also been shown to correlate with the duration of organ failure
(71,72,151).When organ failure is corrected within48h,
mortality was clo to0.When organ failure persisted for
more than48h,mortality was36%(72).chine festival
Several reports have pointed out that a pleural effusion
obtained on chest X-ray within thefirst24h of admission
correlates with greater verity in terms of necrosis or organ
failure(84)or greater mortality(75,86).Additionally,the
prence of infiltrates on chest X-ray within24h has been
associated with greater mortality(75,85,86).
Several reports have indicated that gender has no prognos-
tic significance(31,46,73,83,87,91,165).Furthermore,
etiology has also been shown to have no prognostic signif-
weficance(46,53,60,61,75,83,87,91,168)other than one
report that indicated that patients with alcoholic pancreatitis
in theirfirst episode of pancreatitis have a greater need for
intubation and greater prevalence of pancreatic necrosis(74).
In three reports(82,83,171),almost all deaths in acute pancreatitis occurred during thefirst two episodes,fewer in the third episode.Studies in the future should stratify pa-tients on the basis of number of prior episodes to confirm this obrvation.In one report(172),but not in another(83),a short interval between ont of symptoms and hospitalization correlated with more vere dia,presumably becau ab-dominal pain was particularly inten among patients with early spread of inflammatory changes in the retroperitoneum and elwhere that would cau early third space loss. DIAGNOSTIC GUIDELINE II:DETERMINATION OF SEVERITY BY LABORATORY TESTS AT ADMISSION OR≤48H
The two tests that are most helpful at admission in distinguish-ing mild from vere acute pancreatitis are AP ACHE-II score and rum hematocrit.It is recommended that APACHE-II scores be generated during thefirst3days of hospitalization and thereafter as needed to help in this distinction.It is also recommended that rum hematocrit be obtained at admis-sion,12h after admiss
ion,and24h after admission to help gauge adequacy offluid resuscitation.
Level of evidence:III
The AP ACHE-II verity of dia classification system includes a variety of physiologic variables,age points,and chronic health points,which can be measured at admission and daily as needed to help identify patients with vere pan-creatitis(1,7,Table6).A variety of reports have correlated a higher AP ACHE-II at admission and during thefirst72 h with a higher mortality(<4%with an AP ACHE-II<8 and11–18%with an AP ACHE-II>8)(31,46,52,72,83, 128,147).There are some limitations in the ability of the APACHE-II score to stratify patients for dia verity.For example,in one report,there was no sharp cutoff between interstitial and necrotizing pancreatitis(52).In three reports, APACHE-II scores were not statistically different among pa-tients with sterile and infected necrosis(66,83,134).In one recent report,AP ACHE-II generated within thefirst24h had a positive predictive value of only43%and negative predic-tive value of86%for vere acute pancreatitis as compared to the48-h Ranson score of48%and93%,respectively(53). The advantage of the AP ACHE-II score was the availability of this information within thefirst24h and daily(53).In general,an APACHE-II score that increas during thefirst 48h is strongly suggestive of the development of vere pan-creatitis,whereas an APACHE-II that decreas within the first48h strongly suggests mild
pancreatitis.
Ranson signs have been ud for many years to asss verity of acute pancreatitis but have the disadvantage of requiring a full48h for a complete evaluation.In general, when Ranson signs are<3,mortality is0–3%(46,86,145); when≥3,11–15%(46,86,145);when≥6,40%(46).How-ever,a more recent comprehensive evaluation of110studies concluded that Ranson signs provided very poor predictive power of verity of acute pancreatitis(173).In two studies,
