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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_725_Библиотеки_им_академика_М_И_Перельмана
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pancreatitis(e.g.hypovolemia)butfrom its late sequelae (e.g. SIRS,sepsis,MOF).But
beware of the patient coming in with early ACS-induced renal and respiratory failure
after undergoing massive fluid resuscitation. Measure the IAP, the patient might need
earlydecompressivesurgery!
The 4-week approach to the management of acute
pancreatitis( Figure19.1)
1stweek:inflammation
About85%ofpatientswithacutepancreatitishavethemildformofthe
disease.Inthepastweusedtoadmitthesepatientstotheward,keeping
them starved and inserting a nasogastric tube, and treating the pain,
nausea and delirium with medications. In most cases, the patient
recovered within a few days and was discharged.These days we treat
thesymptomswithmedications,startoralfeedingassoonasthepatient
tolerates it, and look for signs of severe acute pancreatitis hoping to
recognize it early. If all is going well, the patient has mild acute
pancreatitis (a ‘1-week disease’) where the inflammation has resolved
withoutmajorsystemicorlocalcomplications.
Anysignsofcontinuousseverepain,restlessness,respiratorydistress,
decreasing urine output, greatly distended abdomen, increasing CRP
levels, or increasing IAP could indicate that the inflammatory process
continuesandthepatientwillprogresstothesecondstage:necrosis(see
below‘2ndweek’).Remember:mildacutepancreatitisismaximallya
7-daydisease.Anythingthatlastslongerisnotsomild…
OK, time for a little theory: MOF is a consequence of excessive
activation of a systemic inflammatory response cascade, where
inflammatory mediators induce end-organ endothelial cell activation
leadingto increasedpermeability.Leakingmicrovesselscause alossof
intravascular fluid and in conjunction with vasodilatation lead to
hypotension and shock. Accumulation of inflammatory cells in tissues,
increasedinterstitialfluidandactivationofcoagulationwithmicrovascular
thrombosis further impair oxygen supply of tissues (OK, now you can
wakeup!).
Figure19.1.Severeacutepancreatitis:weekbyweek.
TheclinicalmanifestationofallthisisMODSthatdevelopsearly
during the course of acute pancreatitis. Over half of patients with
severeacute pancreatitishave signsof organdysfunction onadmission
— most developing within the first 4days. So, whenthat happens, get
yourpatienttotheICU!
Besides monitoring and supporting organ dysfunction as in all
ICU patients, below are some specific comments about patients
withsevereacutepancreatitisintheICU.
Fluidresuscitation
In the past, aggressive fluid therapy during the early phase ofacute
pancreatitis was one of the dogmas we followed religiously (God have
mercyontheresidentwhohadnotorderedatleast5-10Loffluidforthe
patient). Of course the rationale behind fluid resuscitation is sound: to
correcthypovolemiacausedby‘thirdspace’fluidloss;however,ortoput
itsimply:toolittlefluidleadstohypovolemiaandorgandysfunction,
too much fluid can cause tissue edema and intra-abdominal
hypertension (IAH). Our current fluid resuscitation goals are
summarizedin Table19.2.
Enteralnutrition
Fasting does not help, and it does not alleviate the inflammatory
response or ‘put the pancreas to rest’. Enteral feeding (a product of
millions of years of evolution) is superior to parenteral feeding,
preventsbacterialovergrowthintheintestineandreducesbacterial
translocation, reduces the risk of systemic infections, organ
dysfunctionandmortality.The only contraindication is an inability
toeatbecauseoftheassociatedileusorgastricoutletobstruction.
So,offerfood toa consciouspatientifitistoleratedwithoutvomitingor
aggravatingpain.
Inaventilatedandsedatedpatientthisiswhatwedo:
•
Tryanasogastrictubefirstandstartfeeding.
Ifgastricresidualis>250ml/6hr,insertaself-advancingnasojejunal
•
tubeoraskyourendoscopyfriendtoinsertone.
•
Thenstart feeding with10ml/hrand increase graduallyuntilcaloric
needsaremet.
•
Avoidexceeding60ml/hr.
Enteralfeedingisprobablymorebeneficialinreducingtheriskof
infectiouscomplicationsthanprophylacticantibiotics,souseit!
Prophylacticantibiotics
Thereare manyrandomized controlledtrials andprobably evenmore
meta-analyses(BTW—“Meta-analysisisto analysisasmetaphysics to
physics” said H. Harlan Stone) and systematic reviews, that try to
convinceusthatprophylacticantibioticsdonotbenefitpatientswithacute
pancreatitis. Acknowledging the limitations of the trials and that
patientswithorganfailurearesusceptibletoinfections,webelieve
(not evidence but maybe error-based medicine) that the use of
prophylactic antibiotics in patients with severe pancreatitis is
justified. We base our indication for starting antibiotics on clinical
judgmenttakingintoaccountthepresenceofSIRS,IAH,hyperglycemia,
lowplasmacalcium,highcreatinineorothersignsoforgandysfunction.If
itturns out thatthe patient hasmild acute pancreatitis,it is quiteOK to
terminatetheantibiotics,noharmdone.Westartwithcefuroximeunless
contraindicated(allergy).Youcanuseyourlocalsoupdujour.
Whoneedssurgeryonweek1?
Apartfromsurgicalorendoscopicinterventionsrequiredforgallstoneassociated pancreatitis (see Chapter 20, Section 3), there are very
fewreasonstooperateonpatientswithsevereacutepancreatitisin
theearlystage:
•
Abdominal compartment syndrome (ACS). The combination of
excessive fluid resuscitation and capillary leakage leads to tissue
edema of the abdominal and retroperitoneal organs, and ascites
formation.Intestinalparalysis(ileus)usuallyaddstotheincreaseof
the intra-abdominal volume leading to IAH. For general diagnosis
and management of IAHand ACS,see Chapter 33. When IAH
(defined as IAP ≥12mmHg) develops, non-operative methods to
decrease IAP should be tried first to prevent progressionto a fullblown ACS. If non-operative management, including
percutaneousdrainageofpancreaticascites,failstoreducethe
IAP(goalAPP>60mmHg),surgicaldecompressionisindicated.
Unlike some other indications for an open abdomen (trauma,
peritonitis, bowel ischemia), in acute pancreatitis surgical
decompressionusuallyleadstoanopenabdomenofseveralweeks’
duration. However, with the new methods of open abdomen
management, such as the vacuum-assisted closure (VAC) with
mesh-mediated fascial traction, the delayed fascial closure rates
approach90%withaverylowentericfistularate.
•
Bleeding.Bleeding—usuallyfromthenecroticprocessaroundthe
pancreaserodinganartery—isararecomplicationinsevereacute
pancreatitis, but when it occurs it requires prompt management,
preferablyby angiographic embolization.Sometimes, however,you
areforcedtogoinandpackthebleedingleavingtheabdomenopen
and then do a reoperation 2 days later to remove the packs.
Obviously,hemorrhage inneed ofhemostasis may develop during
thesubsequentweeks.
•
Colon necrosis (actually, this complication is more common later
on…). Necrosis of a part of the transverse colon in acute
pancreatitis is associated with high mortality and is difficult to
diagnose until perforation occurs. Gas bubbles in the colonic wall
seenonCTcanbeausefulhint.Colonnecrosisisprobablycaused
byretroperitonealspreadofthenecrotizingprocesstothecolonwith
fat necrosis and pericolitis. Usually, the inner layers of the colon
remain viable longer.The commonestsite of colon necrosis isthe
adjacent transverse colon — caused by thrombosis of the middle
colic artery branches involved in the peripancreatic necrosis (
Figure 19.2). We have also seen cecal perforations — probably
aggravatedbycolonicdilatation( Figure19.3).Trytoidentifyany
necrosis(gasbubblesandothersignsofnecrosisinthecolon
wall on CT) before it progresses to frank perforation and
contaminationoftheperitonealcavity.Atsurgeryremovalofthe
affectedsegmentisperformed. Primarycolonicanastomosis under
thesecircumstancesisrisky,andacolostomyisabetteroption.
Figure 19.2. Necrosisof thetransverse colon. The necrotic area is between my (on the
left)andmyassistant’sthumbs.
Figure19.3.Patchynecrosisofthececum.
2ndweek:necrosis
Thenecroticprocessinandaroundthepancreasstartstomanifestby
theend ofthefirst week,and theseverity(and theprognosis)depends
on the quantityand extent of the necrotic tissue. A CTscan (with i.v.
contrastnowiftherenalfunctionisnormal)canshowtheextentof
the necrosis. There are classification systems based on the CT
evaluation (the first one developed in Finland by the radiologist Leena
Kivisaari), such as the Balthazar classification (look it up), but the
physiologicalstateandorganfunctionsare better determinants of
severity.Fluidcollectionsaroundthepancreasandinthelessersacare
common. We used to call them pseudocysts, but acute
peripancreatic fluid collection is a more accurate term. They may
resolve spontaneously and as such require no treatment. If the
necroticcollectionsremainsterile,thereisnoreasontooperateat
thisearlystage.So,bepatienteveniftheintensivistsgiveyouthe
typicallook(whilethinking):“Whyishenotgoingtooperate,weare
tiredandboredofthis…”(see Figure19.4).
Figure 19.4. Assistant: “Prof, let’s operate for God’s sake! His pancreas is dead!”
Professor:“Areyou animbecileorwhat?Be patient!We’lloperateperhapsnext month.
Nowgetmesomemorevino!”
3rdweek:infection
The diagnosis of infected necrosis is difficult. Even fine-needle
aspiration (FNA) of the necrosis, usually performed with ultrasound
guidance,hasafalse-negativerateof20-25%.
Clinical signs of sepsis are too non-specific for definitive diagnosis,
although a new increase in the CRP value without any other good
explanationmightalertyoutolookforinfectednecrosis.GetanewCT!If
you are lucky, gas bubbles in the CT scan means infection but
unfortunately,theyarepresentinlessthan10%ofcases.
4thweek:the(surgical)actionreallystartsnow
WhatdoyouseeonCT?
Figure 19.5. Abdominal CT showing walled-off necrosis (WON). Note the encapsulated
collection of pancreatic and/or peripancreatic necrosis with a well-defined, enhancing
inflammatorywall.
AccordingtotheupdatedAtlantaclassification2012:
•
Peripancreatic collections associated with necrosis are termed
acutenecroticcollection(ANC)andwalled-offnecrosis(WON).
In the early phase poorly demarcated acute peripancreatic fluid
collections are commonly seen on CT scan. They are
homogeneous, confined to normal fascial planes, can be multiple,
usually remain sterile and resolve spontaneously without
intervention.So,don’tworryaboutthem.
•
Pancreatic pseudocyst refers to a well-defined fluid collection
containing no solid material. The development of pancreatic
pseudocystisrareinacutepancreatitis,and isoften confusedwith
ANC. However, it may form many weeks after operative
necrosectomyduetolocalizedleakageofadisconnectedduct(see
below)inthenecrosectomycavity.
•
ANC (‘early’) is a collection seen during the first 4 weeks and
containingvariableamountsoffluidandnecrotictissueinvolvingthe
pancreaticparenchymaand/orperipancreatictissues.
•
WON (‘late’) is a mature, encapsulated collection of pancreatic
and/or peripancreatic necrosis with a well-defined, enhancing
inflammatory wall ( Figure 19.5). The maturation takes usually 4
weeks or more after the onset of acute pancreatitis. (If you have
problems remembering these, think about Nelson Mandela and
“ANCwonin40years”.)
Indicationsandtimingforinterventions
According to the International Association of Pancreatology and the
American Pancreatic Association evidence-based guidelines for the
management of acute pancreatitis2, the indications for intervention
(surgical,radiologicalorendoscopic)innecrotizingpancreatitisare:
•
Clinically suspected or documented infected necrosis with
clinical deterioration, or ongoing organ failure for several
weeks.
•
Ongoinggastric outlet,intestinal, orbiliary obstructiondue tomass
effectofWON.
•
PatientnotgettingbetterwithWONbutnoinfection(after8weeks).
•
Disconnectedductsyndrome(fulltransectionofthepancreaticduct)
withpersistingsymptomaticcollectionwithnecrosiswithoutsignsof
infection(>8weeks).
So you see that the timing of intervention is usually postponed until at least 4 weeks
after the initial presentation to allow the WON to be formed. As listed above,
recommendationfor someoftheotherindicationsismorethan8weeks.Thisrequires
lotsofpatience!
Treatment
In patients with suspected or confirmed infected necrotic pancreatic
tissue, the Dutch3 have shown that by using the so-called ‘step-up’
strategy consisting of initial percutaneous drainage followed, if
necessary, by minimally invasive retroperitoneal necrosectomy,
open surgical procedures can be avoided in about one-third of
patients.
Normally we leave the early fluid collections alone for the first 2-3
weeksunlesscausingmajorobstructiveproblemsbycompression.Ifwe
suspect that they are infected, wethen usethe step-upprocedure and
ask our ultrasonographers to put a drain into the collection. We take
bacterial samples and, if positive, we keep the drain and if necessary
proceed to necrosectomy later on, if the drainage procedure is
inadequate(asjudgedbydeterioratinginfectionandorganfunction).Ifit
is sterile, we removethe drain after afew days to avoid drain-induced
contamination/infection of the necrotic collection. We have one or two
patients like this in the ICU at any given time, and we follow the plan
describedaboveandwaitforthebacterialresult.
Howtodoanecrosectomy
Of course, there are several ways of doing a necrosectomy ranging
from minimally invasive to ‘maximally invasive’ techniques, the choice
dependingonthesizeandlocationoftheWON,thepresenceorabsence
of a disconnected duct, and the expertise available. So ask: open or
minimal access pancreatic necrosectomy? Transperitoneal or
retroperitoneal?Closetheabdomenorleaveitopen?Inreality,you
dowhatyouknowbestbutifpossible,tailorthe proceduretothat
which benefits the patient most. It is always useful to have more
thanoneoption.
Endoscopicvariationsforthemanagementofperipancreaticnecrotic
collectionshavebeenintroducedandincludeendoscopicretroperitoneal
drainageorlumboscopicnecrosectomy,andpercutaneousnecrosectomy
and sinus tract endoscopy.The value ofthese techniques isstill under
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