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present, an anti-ulcer procedure can be safely performed: blood
pressure >90mmHg, operation within 48 hoursof perforation,and
lack of associated medical illnesses. We found the APACHE II
1
scoring system ( Chapter 6) useful in this situation as patients with
perforated ulcers with scores of less than 11 can tolerate a definitive
procedureofanymagnitude.Conversely,inpatientswithhigherAPACHE
IIscores,thesimplestoperationshouldbeperformed.
Whichdefinitiveprocedure?
Ideally, in an emergency you should choose theanti-ulcer procedure
withwhichyouaremostfamiliarintheelectivesituation.Theproblemis
thattodayyouandotheryoungsurgeonsaredeprivedofexperiencewith
elective anti-ulcer operations. Based on our philosophy to avoid, if
possible, a gastric resection for a benign process, and on results of
electiveulceroperations(goodoldhistory!),werecommendanoperative
policywhichtailorsthedefinitiveproceduretothespecialsituation as
discussedinthefollowingsection.Whateveryoudopleaseremember
thatifyourpatientissickandyouarenotaskilledgastroduodenal
surgeon — forget about the definitive procedure. Just patch the
holeandgetout!Anyway,itseemsthatinafewyearsnosurgeonable
todoavagotomywillbestillpracticing.Soperhapsinfutureeditionsof
thisbooktherewillbenochapterdedicatedtoperforatedpepticulcer;or
theonlyoperativeoptionmentionedwillbeomentopexy.Infact,afewof
my co-editors suggested that I remove this section altogether. But not
yet…
Specialproblems
These are the situations which may require more than simple
closure:
•
‘Kissing’ ulcers: coexisting active UGI bleeding suggests the
possibility of ‘kissing’ ulcers — the anterior perforated, the
posterior bleeding. Simple closure of the former, without
hemostasis for the latter, could lead to a severe postoperative
hemorrhage. In such circumstances enlarge the duodenal
perforation into a duodenotomy and explore the inside of the
duodenum.If a bleeding posterior ulcer isfound,suture-transfix its
baseasdescribedinthepreceding Chapter17.
•
Perforatedgiantulcers: while omentopexy can be used to repair
most perforated DUs, a giant perforated DU may create a huge
anteriorbulbar-pyloricdefect,whichisnotamenabletosafeclosure
andthusmandatespartialgastrectomy. In our hands this would
bea Billroth I gastroduodenostomyas depicted in Figure17.2 in
thepreviouschapter.
•
Perforated gastric ulcers: these are usually larger than the
duodenalones.Forthosepositionedonthegreatercurvatureofthe
stomach, a wedge resection ofthe ulcer, handsutured orstapled,
may be easier and safer than omentopexy. For chronic and large
lesser curvature ulcers, omentopexy is notoriously difficult and
unsafe; partial gastrectomy may serve the patient better.
Perforationsofmalignantgastriculcersareveryrareinthewest(but
inIndia,forexample,many gastric perforations are malignant). Be
thatasitmay, ifwe decidetopatchagastricperforationwewould
take a fewbiopsies from its edges before closing it. If positive for
cancer,anelectivereoperationfor‘oncological’gastrectomymaybe
necessary.
•
Pyloric obstruction: perforated DUs are rarely associated with
chronic narrowing of the gastric outlet. But if the patient gives a
history of prolonged postprandial vomiting and/or at operation his
stomach appears dilated and thickened, consider that possibility.
Insertyourindexfingerthroughtheduodenalperforationandupthe
pylorus,or feedin aFoley catheterandcheckwhetherthe inflated
balloon (5cc) passes easily through the pylorus. Documented
pyloric stenosis would demand the addition of some form of
drainage procedure (pyloroplasty or gastrojejunostomy). Whether
youwishtoaddatruncalvagotomyisuptoyou.
•
Intractablecases:selectedpatientswithaclearhistoryofchronicity
orintractability(e.g.arecurrentperforation),withnoeasyaccessto
healthcareandmedications may benefit from a definitiveanti-ulcer
procedure. That surgeons in London or Houston no longer find
indications for acid-reducing procedures does not mean that there
arenopatientsinTbilisiwhowouldbenefitfromit.
Non-operativemanagementofperforatedulcers
A non-operative approach consisting of nil per mouth, nasogastric
suction, systemic antibiotics, and acid secretion inhibitors, has been
proven effective by a few enthusiastic groups. The sine qua non for
successisthespontaneoussealingoftheperforationbytheomentumor
otheradjacentstructures;ifthisoccurs,anon-operativeapproachwould
besuccessfulinthemajorityofcases.
Non-operativetreatmentmaybeofparticularvaluefortwotypes
ofpatients:the‘latepresenter’andthe‘extremelysick’.
•
The ‘late presenter’ comes to you a day or more after the
perforationoccurred,withanalreadyimprovingclinicalpictureand
minimal abdominal findings. This, together with radiographic
evidenceoffreeair, hints at a localized and spontaneously sealed
perforation.Non-operativetreatment,followingaGastrografin®UGI
study, or contrast CT, to document that the perforation is sealed,
shouldbesuccessfulinmostinstances.
•
The ‘extremely sick’ are the other candidates for conservative
therapy: those in whom the risk of any operation could be
prohibitive, such as the early post-massive myocardial infarct
patient,theCOPD(chronicobstructivepulmonarydisease)gradeIV
patient,orthepatientwithanAPACHEIIscoreover25.Alsointhis
group, however, conservative treatment may be successful only if
the perforation is sealed and radiographically proven to be so. Of
course,localized collectionsorabscesses developingat the siteof
the sealed perforation can be drained percutaneously under CT
guidance( Chapter46).
Leaksaftertheoperation?
Ifyouhaveperformedaproperomentopexyyoudonot need to
bother reading about how to deal with leaks. However, series of
patients developing leaks from the perforation repair sites are being
reported—reflecting,asmentionedabove,afaultyoperativetechnique,
mostly laparoscopic but also ‘open’. Details on how to manage such
leaksyouwillfindinourbookoncomplications2.
Letusnotforget:
…a course of anti-Helicobacter antibiotics after the operation,
combined with appropriate acid-reducing agents. High-risk elderly
patients may need acid suppression for the rest of their lives. The
durationofsuchmanagementinyoungerpatients,andwhethertheywill
bere-infectedwiththeulcerogenicbacteria,iscontroversial.
Finalwords…
Patchaperforatedulcerifyoucan.Inthevastmajorityofpatientsthis
ispossible,butifnotthenyoumustresect.Consideraddingadefinitive
anti-ulcerprocedureonanextremelyselectivebasis(almostnever),and
do not forget that a non-operative approach is possible, beneficial and
indicatedinselectedpatients.Whateveryoudo,largestudiesshowthat
one-thirdofthesepatientswillbedeadwithin5years—thesamefactors
whichledtotheperforationshortentheirlives.
“Wehaveno responsibility to such patientsbutto save
their lives. Any procedure, which aims to do more than
this, can quite significantly be considered meddlesome
surgery.Wehavenoresponsibilityduringthesurgeryto
carry out any procedure to cure the patient of his
duodenalulcer.”
RoscoeR.Graham
1
AcutePhysiologyandChronicHealthEvaluationII.
2
Tang WH. Leaking gastrointestinal anastomoses — Stomach and duodenum. In: Schein’s
CommonSense Prevention and Managementof Surgical Complications.Shrewsbury,UK:
tfmpublishing,2013;Chapter6.3:116.
Chapter19
Acutepancreatitis
AriLeppäniemi
Duringmillionsofyearsofevolutionthepancreaswandered
totheretroperitoneumfora reason;surgeons shouldthink
twicebeforemessingwithit!
In this chapter I will deal with acute pancreatitis, using alcoholic
pancreatitisasthemainexample.Foradditionalemphasisongallstonebiliarypancreatitisread Chapter20,Section3.Abbreviationsarelisted
in Table19.1.
Nowthatyouhavememorizedbyheartalltheabbreviations,youareallowedtocontinue.The
Editors
Theincidence of acutepancreatitisvaries significantlyandcan be as
high as 102/100,000 population in countries such as Finland where
alcoholisthemostcommonetiologicalfactor(andthemainsourceoffun
exceptsaunaandfishing);gallstonesarethenextmostcommonetiology.
Followingthese twocauses(accounting for70-80% of cases)there are
manyothers:metabolic(hypercalcemia,hypertriglyceridemia),externalor
iatrogenic trauma (ERCP), many drugs (look at Google — you will be
surprisedtoseehowmanydrugshavebeenimplicatedintheetiologyof
acutepancreatitis),infections,postoperativeconditions(cardiacsurgery),
anomalies (pancreas divisum), tumors, hereditary and autoimmune
diseases.Ohyes,don’tforgetsnakebites!
In daily practice, outof those rare etiologies,post-ERCPpancreatitis
seemsthemostcommon.Inallothercasesaskagainaboutalcohol
use…J,and onlythenclassifyitas‘idiopathic’,meaning youhave
noidea what caused thisattack ofacutepancreatitis. However,in
older patients it is important to rule out an underlying pancreatic
neoplasmwithafollow-upCTwhentheinflammationhassubsided.
Inanormal(Finnish)generalhospitalED,about3-4%ofpatientswith
anacuteabdomenhaveacutepancreatitis.Foradifferentialdiagnosis,
rounduptheusualsuspects,suchasperforatedpepticulcer,gastritis,
reflux esophagitis, biliary colic, acute cholecystitis, acute mesenteric
ischemia,intestinalobstruction,acutehepatitis,rupturedabdominalaortic
aneurysm, inferior myocardial infarct, basal pneumonia, etc., and
remember that the clinical picture of severe acute pancreatitis
resembles peritonitis. Often a CT (we do not use i.v. contrast in this
situation — but if you do then check thatrenal function is adequate —
contrastisusedatalaterstagetolookforpancreaticnecrosis)isneeded
toexcludepancreatitis(andpinpointanotherdiagnosis)beforeoperating
onapatientwithclinicalperitonitis.But we’llget tothe diagnosticslater
on…
Naturalhistory
Following the initial triggering factor causing acinar cell injury and
intrapancreatic activation of the pancreatic proenzymes, a local
inflammationofthepancreasactivatesinflammatorycellsandtherelease
of inflammatory mediators. If this process is not localized, a SIRS
develops.Thisiswhenpatientsarriveatyouremergencyroom.Inmost
cases, the disease is self-limited, requiring only supportive and
symptomatictreatment,butinabout15-20%amoresevereformof
pancreatitis develops leading toMODS characterized by dysfunction
ofthe pulmonary,cardiovascular, renaland otherorgansystems. Inthe
severeformstheperipancreaticfat tissue and sometimes the pancreas
itselfundergoesnecrosis—necrotizingpancreatitis;andifthenecrotic
tissueisinvadedbymicrobes(believedtomigratetransmurallyfromthe
adjacent colon), causing infected pancreatic necrosis, the prognosis
gets instantly much worse, and the patient often requires surgical
intervention.
Clinicalpresentationanddiagnosis
Clinicalfeatures
A history is important. A typical patient with acute pancreatitis in
Finlandpresentswith a history of drinkingabottleofvodka (have
youheardaboutthevodkacalledFinlandiawhichinFinlandcostsmore
thandouble what it costsinthe USA?) a dayforthe last 3 weeks,and
thenhegotsomuchpainthathecoulddrinknomore.Mostsuchpatients
have so-called ‘darts-habitus’— you know the big guys in the pub
throwing darts with their jeans lying low and showing the hairy lower
back….Ofcoursetherearealsoguyswho“onlyhadacoupleofbeers”,
soaskagain.
The other typical patient is a dame (as Humphrey Bogart would
say…) with intolerance to certain foodstuffs (greasy food, apples, etc.)
causing colicky upper abdominal pain but this time it is different, and
feels like a belt around the epigastrium. The problem: a tiny gallstone
migrates to the common bile duct causing at least temporary outflow
obstruction of the bile (and pancreatic juice); the stone itself usually
passesspontaneouslythroughthepapillatotheduodenumandsignsof
biliarystasis areminimaland transient(mild elevation ofliver enzymes,
nodilatedbileductsonultrasound).
In addition to epigastric pain, patients often suffer nausea and
vomiting; fever is uncommon unless there is accompanying cholangitis.
Alcohol-inducedpancreatitisisoftenassociatedwithmentalrestlessness
andsometimesevendelirium.
Besidesassessingthevitalsignsandreactingtoseverephysiological
derangement (as in all severely ill patients), physical examination
typically reveals a distended abdomen, epigastric or generalized
tendernessand absent bowel sounds indicating paralytic ileus. In more
severecases,theabdomenmightbefilledwithpancreaticascites,andin
patients with a delayed presentation the typical signs of necrotizing
pancreatitiswith discoloration around the umbilicus(Cullen’ssign) or at
theloins(Gray-Turner’ssign)canbeseen.
Labwork
Elevatedplasmaamylaselevels(pancreas-specific,threetimesupper
normallimit)confirmsthediagnosisbutbeawarethattheamylaselevels
may have returned to normal if the symptoms have been present for
several days. Therefore, some also measure serum lipase levels that
stay elevated for a longer time. Other abdominal catastrophes can
cause mild elevation of the amylase levels, so when in doubt,
request a CT! CRP is usually significantly elevated in severe acute
pancreatitisbutittakes24-48hoursbeforethathappens.Otherlabtests
suchas bloodcount, livertests, electrolytes,glucose andrenalfunction
(creatinine)are important to complement the overall picture and helpful
when planning treatment. If yoususpect hyperlipidemia as the cause,
check triglycerides. In really sick patients with suspected cellular
hypoperfusion,lactatelevelsandarterialbloodgasesareneeded.
Imaging
IfCTis availableinyourhospital,forget plainabdominal X-rays;they
are not helpful except in some cases to rule out mechanical bowel
obstructionorperforation(ifyoubelievetheabsenceoffreeairisenough
to rule out perforation —I don’t…).Of course,plain filmsand CTmay
show pancreatic calcifications in patients suffering from acute-onchronicpancreatitis.ChestX-raysarehelpfulinalaterphasetoassess
pulmonarycongestionandpossiblepleuraleffusion.
AbdominalCTisthebestdiagnostictoolavailable.Itdetectseven
mild acute pancreatitis (some edema around the pancreas, sometimes
onlyconfinedtotheheadortail).Wehave stopped using oral contrast
andusemostlytapwaterasacontrastmedium.AsImentionabove,we
donotuse intravenouscontrastintheinitialphasetoavoiddamageto
the already stressed kidneys. If severe (necrotizing) pancreatitis is
suspected, a later CT scan with i.v. contrast to assess pancreatic
enhancement and vitality can be used after volume restoration and
confirmationofnormalrenalfunction.
Ultrasonographyis used early as a complementary study to identify
orruleoutcholelithiasis(CTisnotreliableindetectinggallstones)anda
dilatedcommonbileduct,butitisnothelpfulindiagnosingpancreatitis.If
the liver enzymes are elevated and ultrasound shows the presence of
gallstonesand/oradilatedcommonbileduct,weusuallyperformMRCP
toseeifthestoneisstillpresentorhaspassedthoughspontaneously.In
most cases when a persistent stone causes biliary stasis, especially
when associated with a high fever (cholangitis), ERCP and
sphincterotomyareindicatedtoclearthecommonbileduct.
Estimationofseverityandclassification
Althoughacontinuum — ranging from edematous acute pancreatitis,
withmildsymptomslastingacoupleofdays,toacritical,severeformof
necrotizing pancreatitis, with MODS — for everyday clinical purposes
acute pancreatitis can be divided into mild, intermediate, severe and
criticalforms.
It is not always clear in the early stages (when you are in the
emergencyroom)intowhichcategorythepatientbelongs,i.e.what
naturalcoursethediseasewilltake.
Sohowdoweassesstheseverityofthedisease?
•
Theamountorprogressionofamylaselevelsdoesnotcorrelatewith
severity; CRP is better (150mg/L is some kind of threshold for
severeacute pancreatitis),but manifestsa coupleof daystoolate;
other potential markers (procalcitonin, interleukin 10, etc.) are not
(yet)inclinicaluse.
•
Clinical scoring systems such as those described by the late
Ranson,USA,orImrie,Scotland(youprobablydonotrememberthe
timewhenmedicalstudentsknewallRanson’scriteriabyheart),are
inaccurate and not usedanymore. TheAPACHEII score( see
Chapter6) measures nicely the severityof the disease — ascore
higherthan8indicatessignificantphysiologicalderangement.Inour
hospitalweusethe
SOFA
1scoreroutinelytomonitorthedegreeof
organ dysfunction; we rely especially on the cardiovascular,
pulmonary and renal components of this score (and also
measurement of the intra-abdominal pressure [IAP] — see
Chapter33)todetermineifthepatientshouldgototheICUdirectly
fromtheemergencyroom.
•
At the end of the day we classify the severity of acute
pancreatitisbycombiningthelocalandsystemicdeterminants
ofseverity.Thelocaldeterminantsarerelatedtothepresenceor
absenceofperipancreaticandpancreaticnecrosisandwhetheritis
sterileorinfected.Thesystemicdeterminantisrelatedtowhether
thereisorganfailureornotand,ifpresent,whetheritistransientor
persistent. These factors are connected, and the relationship
between necrosis, be it infected or not, and the development of
organdysfunctionhasbeenestablishedinmultiplestudies.Thekey
isthedevelopmentofpersistentorganfailure.Themortalityinacute
pancreatitisismainlyassociatedwithMOFwhereastheriskofdying
isminimalinpatientswithnoortransientorgandysfunction.
So in this day and age patients rarely die from the early-acute manifestation of acute
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