Acute Pancreatitis: Seminar
Acute Pancreatitis: Seminar
Acute Pancreatitis: Seminar
Acute pancreatitis
Paul Georg Lankisch, Minoti Apte, Peter A Banks
Acute pancreatitis, an inammatory disorder of the pancreas, is the leading cause of admission to hospital for Lancet 2015; 386: 8596
gastrointestinal disorders in the USA and many other countries. Gallstones and alcohol misuse are long-established Published Online
risk factors, but several new causes have emerged that, together with new aspects of pathophysiology, improve January 21, 2015
http://dx.doi.org/10.1016/
understanding of the disorder. As incidence (and admission rates) of acute pancreatitis increase, so does the demand
S0140-6736(14)60649-8
for eective management. We review how to manage patients with acute pancreatitis, paying attention to diagnosis,
This online publication has
dierential diagnosis, complications, prognostic factors, treatment, and prevention of second attacks, and the possible been corrected. The corrected
transition from acute to chronic pancreatitis. version rst appeared at
thelancet.com on
November 19, 2015
Introduction In four large retrospective studies, type 2 diabetes
In this Seminar, we provide a comprehensive and increased the risk of acute pancreatitis by 186289 Department of General Internal
Medicine and
balanced account of the advances since the 2008 times.1215 Compared with non-diabetics, the risk was Gastroenterology, Clinical
Seminar in The Lancet on acute pancreatitis,3 highlight particularly high in younger patients with diabetes Centre of Lneburg, Lneburg,
areas of controversy or international dierences in (incidence rate ratio 526 in those younger than 45 years Germany (Prof P G Lankisch MD);
Pancreatic Research Group,
practice, and describe concepts underlying the disease. [95% CI 431642]; 244 in those 45 years and older
South Western Sydney Clinical
The annual incidence of acute pancreatitis ranges from [223266]),15 and the excess risk was reduced by School, Faculty of Medicine,
13 to 45 per 100 000 people (appendix).4 In patients antidiabetic drugs.14 The possibility of incretin-based University of New South Wales,
treated in hospital in the USA in 2009, acute pancreatitis therapies leading to acute pancreatitis is being debated.16,17 Sydney, NSW, Australia
(Prof M Apte PhD); Ingham
was the most frequent principal discharge diagnosis Whether failure of fusion of the dorsal and ventral
Institute for Applied Medical
in gastrointestinal disease and hepatology.5 The pancreatic buds during gestation has any clinical or Research, Liverpool Hospital,
number of discharges with acute pancreatitis as pathological results is unknown. In a group of patients Liverpool, NSW, Australia
principal diagnosis was 30% higher than in 2000. with acute and chronic pancreatitis, the prevalence of (M Apte); and Division of
Gastroenterology, Hepatology,
Acute pancreatitis was the second highest cause of pancreas divisum was similar in those with and without
and Endoscopy, Harvard
total hospital stays, the largest contributor to aggregate idiopathic (75%) and alcoholic (7%) pancreatitis, Medical School, and Brigham
costs, and the fth leading cause of in-hospital showing that pancreas divisum alone does not cause and Womens Hospital, Boston,
deaths, showing the importance of accurate data for the disease.18 However, associations between pancreas MA, USA (Prof P A Banks MD)
the disorder. divisum and mutations of cystic brosis transmembrane Correspondence to:
Prof Paul Georg Lankisch,
conductance regulator (CFTR) of 47%, serine protease
Department of General Internal
Causes inhibitor Kazal-type 1 of 16%, or protease, serine 1 of Medicine and Gastroenterology,
Gallstones and alcohol misuse are the main risk factors 16%, were noted, suggesting a cumulative eect. This Clinical Centre of Lneburg,
for acute pancreatitis (appendix). During 2030 years, conclusion is not straightforward, however, because Reiherstieg 23,
D-21337 Lneburg, Germany
however, the risk of biliary pancreatitis is unlikely to be associations do not necessarily mean causation.
[email protected]
more than 2% in patients with asymptomatic gallstones6 Patients with pancreas divisum and CFTR mutations
and that of alcoholic pancreatitis is unlikely to exceed should be referred for genetic counselling, and See Online for appendix
23% in heavy drinkers.7 Other factors, possibly genetic, endoscopic or surgical therapy should be withheld
therefore probably play a part. Drugs represent an unless randomised studies show benet.19
additional cause of acute pacreatitis8 (panel 1 and Pancreatitis is the most frequent complication after
appendix). endoscopic retrograde cholangiopancreatography (fre-
Smoking might increase the risk of acute pancreatitis.911 quency 35% in unselected patients).20 It is mild or
There is no association between smoking and biliary
pancreatitis, but the risk of non-gallstone-related acute
pancreatitis has been shown to more than double Search strategy and selection criteria
(relative risk 229, 95% CI 163322) in present We searched PubMed for the term acute pancreatitis,
smokers with 20 or more pack-years compared with together with aetiology, pathogenesis, prognostic
never-smokers. Notably, in heavy smokers with a parameters, complications, death, treatment, or
consumption of 400 or more grams of alcohol per month, prognosis. We included articles in English, French, German,
the risk increased by more than four times (412, and Spanish from Jan 1, 2009 to Dec 31, 2013, together with
198860). Smoking duration rather than intensity highly cited older publications that seemed necessary for full
increased the risk. It was benecial to stop smoking, understanding. Moreover, we included several sets of
but only after two decades was the risk similar to guidelines, two of which cover almost the whole range of
non-smokers. These ndings9 could show that smoking acute pancreatitisnamely, those from the American College
is an independent risk factor for acute pancreatitis, but of Gastroenterology1 and the International Association of
residual confounding factors and missing alcohol intake Pancreatology and American Pancreatic Association.2
data are limitations of the study.
Alcoholic pancreatitis
Alcohol is known to exert direct toxic eects on the Stellate cell
ZG
pancreas, but additional triggers or cofactors seem to be activation L
necessary to initiate overt pancreatitis. Early studies Stellate cell GP2
focused on the eects of alcohol on the sphincter of Oddi
as a possible mechanism of duct obstruction leading to Ca2+
inhibitors, cytokines, CFTR, MHC antigens, alcohol- classication recommends that the modied Marshall
metabolising enzymes, oxidant stress-related proteins, scoring system should be used to characterise the
and detoxifying enzymes have not shown an association severity of failure of these three systems. Systemic
with alcoholic pancreatitis. Investigators of a genome-wide complications are dened as exacerbations of
association study reported an association between pre-existing comorbidities, including congestive heart
overexpression of claudin 2 (a tight-junction protein) and failure, chronic liver disease, and chronic lung disease.
increased risk of alcoholic pancreatitis, with the protein Local complications include interstitial pancreatitis
overexpressed on the basolateral membranes of acinar (peripancreatic uid collections and pancreatic pseudo-
cells in these patients.42 However, the functional cysts) and necrotising pancreatitis (acute necrotic
signicance of this nding remains unclear. collections and walled-o necrosis; panel 2). Patients
A nal aspect of pathogenesis is the multitude of who have moderately severe acute pancreatitis might
signalling pathways and molecules that are perturbed need a longer stay in hospital and have a higher
within the acinar cell upon exposure to injurious agents, mortality than patients with mild acute pancreatitis.
but accumulating evidence points to aberrant intracellular Severe acute pancreatitis is characterised by the
calcium signalling as the nal common mechanism for presence of persistent single-organ or multiorgan failure
acinar injury (appendix).43,44 (dened by organ failure that is present for 48 h). Most
patients who have persistent organ failure have
Classication pancreatic necrosis and a mortality of at least 30%.
The Atlanta classication45 is the standard classication of An alternative stratication of acute pancreatitis severity
the severity of acute pancreatitis. The recently published has been proposed, which includes four categories rather
revised classication46 provides denitions of the clinical than three (table 2).47 These are mild (absence of necrosis
and radiologic severity of acute pancreatitis. Clinical severity or organ failure), moderately severe (sterile necrosis and/
of acute pancreatitis is stratied into three categories: mild, or transient organ failure), severe (infected necroses or
moderately severe, and severe (table 2). persistent organ failure), and critical (infected necroses
Patients with mild acute pancreatitis (no organ failure and persistent organ failure). Studies will be needed to
or systemic or local complications) usually do not need ascertain whether it is more clinically relevant to stratify
pancreatic imaging and are frequently discharged within patients into these three or four categories of severity.
37 days of onset of illness. For radiological severity of acute pancreatitis, the
Moderately severe acute pancreatitis is characterised revised classication provides detailed denitions of the
by one or more of transient organ failure (dened as imaging features of the disease. Acute peripancreatic
organ failure lasting <48 h), systemic complications, or uid collections occur within the rst several days of
local complications. Organ failure includes respiratory, interstitial pancreatitis. They are homogeneous in
cardiovascular, and renal failure using the same criteria appearance, usually remain sterile, and most often resolve
as in the Atlanta Symposium of 1992.45 The revised spontaneously. An acute peripancreatic uid collection
that does not resolve can develop into a pseudocyst, which
contains a well dened inammatory wall. There is very
Atlanta classication 199245 Revised Atlanta Determinant-based little, if any, solid material within the uid of a pseudocyst.
classication 201246 classication 201247
Of particular importance is the radiological denition of
Mild No organ failure and no local No organ failure and no No (peri)pancreatic acute necrotic collections and walled-o necrosis.
complications local or systemic necrosis and organ failure
Previously, the site of acute necrotic collections in necro-
complications
tising pancreatitis was thought to include the pancreatic
Moderately severe .. Transient organ failure Sterile (peri)pancreatic
(<48 h) and/or local or necrosis and/or transient parenchyma and peripancreatic tissue or, on rare occas-
systemic complications organ failure (<48 h) ions, only the pancreatic parenchyma. It is now recognised
without persistent organ that acute necrotic collection can include only the
failure (>48 h)
peripancreatic tissue. Patients with peripancreatic necrosis
Severe Local complications and/or Persistent organ failure Infected (peri)pancreatic
organ failure: PaO2 60% or (>48 h):* single organ necroses or persistent
have an increased morbidity and mortality compared with
creatinine 1526 mol/L or failure or multiple organ organ failure (>48 h) interstitial pancreatitis. Acute necrotic collections in necro-
shock (systolic blood pressure failure tising pancreatitis can be sterile or infected. The natural
60 mm Hg) or
history of acute necrotic collections is variable. They can
gastrointestinal bleeding
(>500 mL/24 h) become smaller and, on rare occasions, wholly disappear.
Critical .. .. Infected (peri)pancreatic Most often, acute necrotic collections develop a well dened
necroses and persistent inammatory wall surrounding varying amounts of uid
organ failure and necrotic debristermed walled-o necrosiswhich
Neither Atlanta classications have a fourth critical group; this group is solely in the determinant-based can be either sterile or infected.
classication. *Persistent organ failure is now dened by a modied Marshall score (appendix).48 This revised classication needs to be tested to assess
its clinical usefulness, and is likely to undergo further
Table 2: Denition of severity in acute pancreatitis.
revisions in the future. The appendix lists clinical
presentation and physical examination, and the essential concentrations on admission are not associated with
abdominal and systemic complications of acute disease severity.49 The disease can be serious, even fatal,
pancreatitis. although the enzymes are only slightly increased (<three-
times normal).
Diagnosis
Main diagnostic procedures Laboratory tests
Clinicians are interested in conrmation of the diagnosis In addition to serum amylase and lipase, the following
and exclusion of dierential diagnoses (appendix). In variables should be established on admission: complete
accordance with the revised Atlanta classication, acute blood count without dierential; concentrations of
pancreatitis can be diagnosed if at least two of the following electrolytes, blood urea nitrogen (BUN), creatinine,
three criteria are fullled: abdominal pain (acute onset of serum glutamic pyruvic transaminase, serum glutamic
persistent and severe epigastric pain, often radiating to the oxalic transaminase, alkaline phosphatase, and blood
back); serum lipase (or amylase) activity at least three times sugar; coagulation status; and total albumin. Arterial
the upper limit of normal; or characteristic ndings of blood gas analysis is generally indicated whenever
acute pancreatitis on contrast-enhanced CT or, less often, oxygen saturation is less than 95% or the patient is
MRI or transabdominal ultrasonography.46 Diagnostic tachypnoeic. The frequency of repeat determinations
imaging is essential in patients with a slight enzyme depends on the clinical course.
elevation (appendix). Importantly, pancreatic enzyme
ECG and chest radiograph One such approach is the harmless acute pancreatitis
50% or fewer cases of ST segment elevations and score (HAPS), which enables identication of mild cases
negativities are registered, mainly in the posterior wall, of acute pancreatitis (which is most of them) within
without myocardial infarction. Chest radiographs in 30 min of inpatient admission, even by non-specialists.
two planes can show pleural eusions and pulmonary Two prospective studies,60 one monocentric and the other
inltrates, which are signs of severe disease. Abdominal multicentric, showed that mild acute pancreatitis can be
panoramic radiographs (upright or left lateral position) predicted with 98% accuracy in patients with no rebound
can be used for diagnosis too. Ileus is shown by a sentinel tenderness or guarding and normal haematocrit and
loop (isolated bowel loop in left-upper or middle abdomen) serum creatinine concentrations. Studies from Sweden61
or colon cuto sign (absence of air in left colonic exure and India62 support the accuracy of HAPS. This score
or descending colon). Pancreatic calcications represent thus identies most patients who have neither developed,
proof of chronic pancreatitisie, that the patient is having or will develop, necrotising pancreatitis or organ failure,
an episode of acute superimposed on chronic pancreatitis, and will therefore not need intensive care. HAPS can be
rather than a rst episode of acute pancreatitis. used in the community care setting, in which the treating
physician can triage the patients who need early transfer
CT to more specialised centres for more aggressive
Unenhanced CT scoring systems assess the extent of management and meticulous monitoring.62 The score
pancreatic and peripancreatic inammatory changes might even be able to establish whether the patient could
(Balthazar score50 or pancreatic size index51), or both be cared for adequately and more economically as an
peripancreatic inammatory changes and extrapancreatic outpatient.
complications (mesenteric oedema and peritoneal uid
score,52 extrapancreatic score,53 or extrapancreatic Therapy
inammation on CT score).54 The patients management begins on the emergency
Two CT scoring systems need intravenous contrast ward, where acute pancreatitis has to be conrmed,
agents to establish the presence and extent of pancreatic the risk stratied, and basic treatment initiated. This
parenchymal necrosis. The CT severity index55 combines treatment includes early uid resuscitation, analgesia,
quantication of extrapancreatic inammation with extent and nutritional support (appendix). Patients undergoing
of pancreatic necrosis, whereas the modied CT severity volume resuscitation should have the head of the bed
index56 assigns points for extrapancreatic (eg, vascular, raised, undergo continuous pulse oximetry, and receive
gastrointestinal, or extrapancreatic parenchymal) compli- supplemental oxygen. Supplemental oxygen has been
cations and presence of pleural eusions or ascites. shown to more than half mortality in patients older than
Contrast-enhanced CT is the gold standard for 60 years.63
diagnostic imaging to help to establish disease severity In experimental pancreatitis in the rat, pancreatic
(the appendix contains axial contrast-enhanced CT microvascular perfusion is reduced, which is aggravated
scans of the pancreas of a patient with acute pancreatitis by arterial hypotension.64 The situation in human beings,
on admission and 1, 10, and 20 days later). However, the however, remains unclear. Neither comparisons of
predictive accuracy of CT scoring systems for severity aggressive versus non-aggressive resuscitation protocols
of acute pancreatitis is similar to clinical scoring (4 L vs 35 L within the rst 24 h) nor goal-directed uid
systems. A CT scan on admission solely for severity therapy (goals have included BUN concentration, central
assessment in acute pancreatitis is therefore not venous pressure, haematocrit concentration, heart rate,
recommended.57 An early CT scanie, done within the blood pressure, and urine output) have yielded clear
rst 4 full days after symptom onset (days 04)does results.65 The investigators of one retrospective study
not show an alternative diagnosis, help with the showed that early uid resuscitation was associated with
distinction of interstitial versus necrotising pancreatitis, reduced incidence of systemic inammatory response
or provide evidence of an important complication.58 An syndrome and organ failure at 72 h,66 but too little uid is
early CT scan should therefore be obtained only when just as deleterious as too much. In one study, rapid
there is clinical doubt about the diagnosis of acute haemodilution increased both the incidence of sepsis
pancreatitis, and other life-threatening disorders have within 28 days and in-hospital mortality.67 In another, the
to be excluded. administration of a small amount of uid was not
associated with a poor outcome, but the need for a large
Prognostic variables amount of uid was.68
Existing scoring systems (appendix) seem to have With regard to what should be infused, the recommend-
reached their maximum eectiveness in the prediction ations of the American College of Gastroenterology
of persistent organ failure in acute pancreatitis. (ACG) and International Association of Pancreatology
Sophisticated combinations of predictive rules are more (IAP)/American Pancreatic Association (APA) guidelines
accurate, but cumbersome, and therefore of restricted are very similar: ACG suggests that lactated Ringers
clinical use, and new approaches are needed.59 solution might be preferred to isotonic crystalloid
replacement uid,1 whereas IAP/APA merely state2 that supplementary nutrition. Enteral nutrition was associated
Ringers lactate should not be given to the few patients with a lower risk of complications than parenteral
with hypercalcaemia for initial uid resuscitation. The nutrition, but not with a signicant change in mortality.
two sets of guidelines dier with regard to rate of However, timing is crucial. The investigators of a
infusion, with ACG suggesting a rate of 250500 mL/h systematic review of 11 RCTs showed that when started
and IAP/APA suggesting 510 mL/kg per h. If the ACG within 48 h of admission, but not later, enteral nutrition,
recommendation is assumed to be for a patient weighing compared with parenteral nutrition, signicantly reduces
70 kg, following the IAP/APA guideline would lead to a the risk of multiorgan failure, pancreatic infectious
much higher rate of infusion, of 50700 mL/h. Only ACG complications, and mortality.77 Many studies have
makes a rm recommendation as to when infusion proposed that enteral nutrition should be given via a
should begin, stating that early aggressive intravenous nasoduodenal rather than nasojejunal tube, but a rm
hydration is most benecial in the rst 1224 h and could recommendation cannot yet be given.7881 An initial
have little benet beyond this time.1 attempt at nasoduodenal intubation seems advisable, but
These recommendations are essentially based on a the pancreatic head inammation in severe acute
prospective multicentre randomised study69 in which pancreatitis can cause duodenal stenosis, necessitating
resuscitation with lactated Ringers solution reduced by endoscopic placement. Nausea and vomiting because of
84% during the rst 24 h compared with normal saline. persisting gastroparesis, ileus, or postprandial pain
Infusion started with a bolus of 20 mL/kg bodyweight suggests parenteral nutrition via a central venous catheter.
followed by 3 mL/kg for 812 h. Crucial, however, is Glutamine supplementation has been discussed for
adjustment of the infusion rate depending on the results of patients with critical acute pancreatitis leading to
measurements of intervals of no more than 6 h for at least catabolism. Findings from a meta-analysis of 12 RCTs82
2448 h. One decisive variable is BUN because investigators showed that glutamine supplementation signicantly
have shown that increased BUN concentration at admission reduced the risk of mortality and total infectious
and during the rst 24 h are independent risk factors for complications in parenterallybut not enterallyfed
mortality in acute pancreatitis.70,71 The recommendation has patients, but did not shorten the hospital stay. The
been made to adjust uid resuscitation during the rst 24 h absence of a positive eect of enteral glutamine
on the basis of whether BUN concentration increases supplementation was attributed to the fact that
or decreases.72 glutamine is largely metabolised in the gut and liver so
Pain treatment has absolute priority on admission. that the plasma glutamine concentration is lower after
Unfortunately, ndings from a systematic review enteral than after intravenous administration. An
showed that the randomised controlled trials (RCTs) additional point to note is that treatment with
comparing dierent analgesics were of low quality and antioxidants is ineective.8385
did not clearly favour any particular analgesic for pain A Cochrane review86 showed no evidence that routine
relief.73 Until a conclusive study is reported, the early endoscopic retrograde cholangiopancreatography
prevailing guidelines for acute pain management in the signicantly aects mortality and local or systemic
perioperative setting should be followed.74 complications in patients with acute gallstone pancreatitis,
Patients in high-volume centres (118 admissions per irrespective of predicted severity. The results, however,
year) have a 25% lower relative risk of death than do support present recommendations86 that early endoscopic
those in low-volume centres.75 Patients who do not retrograde cholangiopancreatography should be considered
respond to early resuscitation or display persisting organ in patients with coexisting cholangitis or biliary obstruction.
failure or widespread local complications should
therefore be transferred to a pancreatitis centre (if Management of local complications
available) with multidisciplinary expertise, including Necrosis
therapeutic endoscopy, interventional radiology, and Prophylactic antibiotics are not indicated.8790 Surgical
surgery. Patients with persistent systemic inammatory resection of pancreatic necroses can be achieved by
response syndrome, increased concentrations of BUN or open, laparoscopic, or staged necrosectomy (open-staged
creatinine, increased haematocrit, or underlying cardiac or closed-continuous lavage). These methods do not
or pulmonary illness, should be admitted for compete with, but rather complement, other techniques.
monitoringeither intensive or intermediate care, No guidelines exist, but there is consensus that surgical
depending on availability. All other patients, especially intervention should be doneif at allat a late stage, at
those in whom HAPS60 predicts harmless acute least 2 weeks after the onset of pancreatitis.91
pancreatitis, can be treated on a general ward. More conservative interventions than surgery now
In mild acute pancreatitis, oral feedings can be started predominate92,93 as a result of two pioneering advances.
if there is no nausea and vomiting, and abdominal pain Antibiotic treatment alone can heal infected necrosis.94
has resolved.1 Findings from a systematic review of This is now the rst step when such lesions are shown.
15 RCTs76 showed that either enteral or parenteral Antibiotic treatment is possible in almost two-thirds of
nutrition is associated with a lower risk of death than no patients with necrotising pancreatitis, with a mortality of
7%.95 Seifert and colleagues96 successfully introduced mortality.108,109 If sepsis is suspected, it is reasonable to start
debridement of infected necrosis after fenestration of the antibiotics while waiting for blood culture results. If
gastric wall. This form of intervention has become widely culture results are negative, antibiotics should be
used and other routes of access have been developed, but discontinued to reduce the risk of fungaemia110 or
it should be restricted to specialist centres. Long-term Clostridium dicile infection.72
success can then be achieved in two-thirds of patients.97
Endoscopic transgastric necrosectomy compares favour- Aftercare
ably with surgery.98 Clinical trials are needed to validate Refeeding
the various options for intervention. Basic treatment of acute pancreatitis should be
Van Santvoort and colleagues99 compared step-up continued until the patient shows distinct clinical
management of infected necrosis (placement of improvement (freedom from pain and normal body
percutaneous catheters in addition to treatment with temperature and abdominal ndings). No binding
antibiotics, if necessary followed by minimally invasive recommendation for severe acute pancreatitis exists; the
necrosectomy) with open necrosectomy. This step-up decision is taken on an individual basis. In mild acute
approach reduced new-onset multiorgan failure by 29%. pancreatitis, oral feeding should be resumed as soon as
However, the study was underpowered to detect a possible according to the present European Society for
dierence in mortality. Parenteral and Enteral Nutrition guidelines.111 When and
In patients with walled-o necrosis, physicians should how this feeding should be resumed remains undened.
intervene only in the event of symptoms attributable to The beginning of refeeding certainly does not depend on
the collection (persistent abdominal pain, anorexia, the normalisation of lipase.112 The decision should
nausea, or vomiting from mechanical obstruction or perhaps be left to the patientsie, they can eat when
secondary infection).72 In this case, direct endoscopic they are hungry.112,113 Positive experience with refeeding at
necrosectomy is possible in skilled hands.100 the patients request has been reported with widely
varying diets: unspecied,114 soft diet,115 and full diet
Pseudocyst with116 or without117 fat restriction. Unfortunately,
Prognostic factors for the development of pseudocysts are however, oral refeeding can lead to pain relapse and
alcohol misuse and initially severe disease. Spontaneous therefore to a longer hospital stay (appendix).
resolution occurs in a third of patients with a pseudocyst.
Prognostic factors for this resolution are no or mild Imaging procedures
symptoms, and a pseudocyst diameter of no more than Patients with acute pancreatitis of unknown origin
4 cm.101 Symptomatic pseudocysts can be successfully should undergo endosonography to exclude stones or
decompressed by endoscopic cystogastrostomy with sludge in the gallbladder or bile ducts. Endosonography
endoscopic ultrasound guidance.102 or magnetic resonance cholangiopancreatography can be
indicated to exclude a tumour. Tumour-related acute
Ductal disruption pancreatitis can seem to heal before aring up again.118
Ductal disruption can result in unilateral pleural eusion,
pancreatic ascites, or enlarging uid collection. If the Transient exocrine and endocrine pancreatic insuciency
disruption is focal, placement of a bridging stent via Both exocrine and endocrine transient pancreatic
endoscopic retrograde cholangiopancreatography usually insuciency can occur during healing.119121
promotes duct healing.103 When ductal disruption occurs Pancreatic function should therefore be monitored,
in an area of widespread necrosis, optimum management which is generally normal again 3 months after
needs a multidisciplinary team of therapeutic endoscopists, abatement of acute pancreatitis. Pancreatic enzyme sub-
interventional radiologists, and surgeons.104 stitution is not usually necessary, but can be temporarily
necessary after a severe attack.
Peripancreatic vascular complications Endocrine pancreatic function should be checked after
Splenic vein thrombosis has been reported in up to 20% about 3 months (by fasting and postprandial blood sugar
of patients with acute pancreatitis undergoing imaging.105 concentrations, possibly by HbA1C measurement). Severe
The risk of bleeding from gastric varices is less than 5%, acute pancreatitis is often followed by diabetes mellitus.122
and splenectomy is not recommended. Pseudoaneurysms
are rare, but cause serious complications in 410% of Transition to chronic pancreatitis
cases.106 Mesenteric angiography with transcatheter In a German study,123 over a period of almost 8 years,
arterial embolisation is the rst-line treatment.107 only alcoholics developed chronic pancreatitis,
independently of both severity of rst acute pancreatitis
Management of extrapancreatic complications and discontinuation of alcohol and nicotine. The
Extrapancreatic infections, such as bloodstream infections, cumulative risk of the development of chronic
pneumonia, and urinary tract infections, occur early in up pancreatitis was 13% within 10 years and 16% within
to 24% of patients with acute pancreatitis, and can double 20 years. The risk of chronic pancreatitis in those who
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