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Though probably one of the more challenging emergency
procedures by laparoscopy, this may also be one of the most
rewarding:cuttingasingleadhesivebandcanbeaquickprocedurethat
prevents a closed loop obstruction from quickly progressing to bowel
necrosis. Indeed, some obstruction cases are the result of multiple
adhesions, and extensive adhesiolysis is needed — not a task for a
laparoscopic spring-chicken. But, when laparoscopic adhesiolysis is
successful,theadvantagestothepatientaresignificant:thequickreturn
ofbowelfunction,thereducedriskfornewadhesions,andofcoursethe
wound-associated complications (dehiscence is a real risk after
laparotomy for obstruction, due to the distended bowel and increased
abdominalpressure).
Inordertoachievetheseadvantages,yourtechniquemustbeflawless.
The risk of perforating an obstructed bowel is real, and spillage of the
high-pressure, static contents may lead to an uncontrollable and
irreversible sepsis. Going ‘in reverse’ from the collapsed, distal
bowel,avoidingbowelhandlingasmuchaspossible,andavoiding
theuseofenergysourceswillhelpyouavoiddisaster.
Incarceratedhernia
Commonlyan indicationfor anopen procedure,incarcerated hernias,
whether incisional or inguinal, can be approached laparoscopically.
Indeed,reducingtheincarceratedcontentsbypulling(gently!)is usually
easierthanbypushing,assistedofcoursebythemusclerelaxationofthe
abdominalwall.Theherniadefectcanalsoberepairedlaparoscopically,
but if you find necrotic bowel then conversion, resection and primary
herniarepairisyourbestbet.Ofcourse,ifyouropenherniaskillsare
better than the lap ones in the elective situation this is what you
shoulduseintheemergency.
Trauma
As repeatedly mentioned above, abdominal trauma is not an
indication for laparoscopic surgery, but a few specific conditions
make laparoscopy more appealing. Diaphragmatic laceration is
sometimes difficult to diagnose, and if highly suspected, and no other
indications for abdominal exploration currently exist, laparoscopy, in a
stable patient, is a good alternative (especially on the left side).
Diagnosis, and non-absorbable suture repair are relatively easy. In a
hemodynamically-normal patient it may even be worthwhile to delay
surgery until the next morning — make sure the patient really has no
otherinjuries,andhavetheproceduredonebyyourexpertlaparoscopist,
whodoesn’tliketobemovedoutofhisbedatnight.
Did I forget to mention anything important? What about SILS and
NOTES some crazy cowboysurgeon could ask. Theanswer has been
providedbyothers.
“NOTES (natural orifice transluminal endoscopic
surgery) is NUTS; SILS (single-incision laparoscopic
surgery)isSILLY.”
MarkCheetham
“StupidInnovationbyLaparoscopicSurgeons.”
MarkPleatman
Chapter13
Peritonitis:classificationandprinciplesoftreatment
MosheScheinandRogerSaadia
The mechanical control of the source of infection, while
itselfnonbiologic,determinestheextentofthehostbiologic
responsetothedisease.
RonaldV.Maier
Inperitonitis—sourcecontrolisaboveall.
The finding of inflammation, bowel contents or pus, localized or
dispersed throughout the peritoneal cavity is common at emergency
laparotomy.Howisthisscenariobesthandled?Thischapterwilldiscuss
semanticdistinctions andgeneral aspectsof the surgical treatment.For
themanagementofindividualcausesofperitonitisyouarereferredtothe
specificchapters.
Nomenclature
Inflammation of the peritoneum is termed peritonitis. It is generally
causedby abacterialinoculum. Thisexplains why peritonitisand intra-
abdominal infection (IAI) are used interchangeably. It is important to
note though that these two terms are not synonymous, because
peritonitismayalsobesterileas withthechemicalperitonitisof early
perforation of a peptic ulcer or inadvertent infusion of enteral feeding
throughamisplacedjejunostomytube.
Herearesomedefinitionstoconfuseyoumore:
•
Intra-abdominalinfection. Foracondition to be labelledIAI, both
theintraperitonealpresenceofmicro-organisms(ortheirtoxins)and
the inflammatory response of the peritoneum are required. A
purulentexudateisoftenfoundatlaparotomy.
•
Peritoneal contamination is different. It consists merely of the
soilingoftheperitonealcavitybyafluidrichinmicro-organisms,as
intheimmediateaftermathof a penetrating intestinal injury, before
an inflammatory response has taken place. Peritoneal
contamination occurs commonly, to varying degrees, in the
course of routine elective surgery when the lumen of the
gastrointestinaltractisbreached.
•
IAIcanbediffuseasingeneralizedperitonitisorlocalizedasin
intra-abdominal abscesses. The latter develop as a result of
effective host defences and represent a relatively successful
outcome of peritonitis.The mainstay of treatment is drainage. For
how, and by which route, find out in the dedicated chapter (
Chapter46).Notethattheseverityspectrum,thelocationofIAIand
theeaseofits‘sourcecontrol’greatlyimpactthemanagementand
outcome; so for example, locally perforated appendicitis does not
mandate the same duration of antibiotic administration as infected
pancreaticnecrosis.
•
Abdominal sepsis is still a term used very commonly but we,
semanticnudniks,donotlikeit.Accordingtomodernconsensus
‘sepsis’meanstheconjunctionofboththe host’sresponseto
infection (SIRS) and a source of infection. Thus, the use of
‘sepsis’, in the abdominal context, wouldnot take intoaccount the
importantinitial local inflammationwithintheperitonealcavity. This
peritonealresponseisanalogous,at alocal level,with SIRSat the
systemic level, because it represents, likewise, a non-specific
inflammatoryresponseofthehosttoavarietyofnoxiousstimuli,not
necessarily infectious. Strictly speaking, therefore, local
contamination,infectionandsepsisrefertodifferentprocesses.Yet,
theymaycoexistinthesamepatient,developingsimultaneouslyor
consecutively—acontinuum.Abdominalcontaminationmayleadto
infection, which is invariably associated with a systemic
inflammatory response. Significantly, residual abdominal
inflammation or indeed the systemic response (fever,
leukocytosis) may even persist after the intraperitoneal
infection has been eradicated. Once set in motion, the
inflammatorycascadecannotbestoppedsimplybyturningoff
thetrigger.
Classificationofperitonitis
Secondaryperitonitis
This is caused by a breach in the anatomical integrity of a hollow viscus (e.g.
perforationortransmuralnecrosis).Itisusuallycharacterizedbyanaerobicandanaerobic
polymicrobial inoculum, reflecting the flora of the gastrointestinal tract. Management of this
condition is the ‘bread and butter’ of the general surgeon. Examples include perforated
appendicitis,perforateddiverticulardiseaseof thecolon,strangulatedobstructionofthesmall
bowel and ruptured tubo-ovarian abscess. It is largely because of secondary peritonitis
thatyou should train yourselftobecome an expert inthejudicious use of antibiotics!
(Tryatleasttobeasknowledgeableasyourlocalinfectiousdiseaseguru…).
We draw your attention to a particularly important distinction.
Secondaryperitonitisis saidtobe‘community-acquired’whenitisthe
reasonforthehospitaladmission(e.g.thepatientwalksthroughtheER
doorswithabdominalpainduetoaperforatedappendicitis).Ontheother
hand,‘nosocomial’secondary peritonitis isamorbid event occurringin
analreadyhospitalizedpatient(e.g.ischemicperforationofthecolonina
ventilated patient treated for severe pneumonia or the patient with
‘postoperative peritonitis’ due to a leaking anastomosis). These two
entitiesdiffersignificantly—thediagnosisofperitonitisismucheasier
tomakeintheERthaninanICUpatientwithmultiplecomorbidities;the
antibiotic treatment is standard broad-spectrum in community-acquired
peritonitis, whereas it needs tobe tailored to a hospital-acquired,more
pathogenic and often unexpected flora in the patient with nosocomial
peritonitis. Finally, the prognosis is much less favourable in the
nosocomialvariety.
Primaryperitonitis
In contrast to secondary peritonitis, this is not caused by a loss of
gastrointestinal wall integrity and is not associated with leakage of
intestinal contents into the peritoneal cavity. The responsible micro-
organism, typically single (as opposed to the complex flora of
secondary peritonitis), originates from a source outside of the
abdomen.In younggirls, it is usuallya Streptococcus gaining access
viathegenitaltract.Inpatientswithcirrhosis,Escherichiacoliisthought
tobeablood-borneagentinfectingthepre-existingascites—acondition
referred to as spontaneous bacterial peritonitis. In patients receiving
peritoneal dialysis, Staphylococcus migrates from the skin along the
dialysiscatheter.
In patients with a known predisposing factor (e.g. ascites
associatedwithchronicliverdisease),suspectedprimaryperitonitis
can be diagnosed by paracentesis (polymorphonuclear count in the
asciticfluidgreater than 250 cells/mm3); a positive culture confirms the
diagnosisbut,evenwithanegativeculture,antibiotictreatmentshouldbe
instituted. Whenever possible, a diagnostic exploratory laparotomy
should be avoided because of its prohibitive mortality; in an
advancedcirrhoticpatient,itoftenamountsto anautopsy in vivo.
Initial antibiotic treatment is empiric, until results of bacteriological
sensitivitiesbecomeavailable.
Primary peritonitis in patients without a known predisposing factor is
extremely rare. It is usually diagnosed at laparotomy for an ‘acute
abdomen’ revealing an odorless exudate without an apparent source.
The diagnosis is reached by exclusion after a thorough abdominal
explorationand is confirmedby a Gramstainand culture whichusually
isolatesasolitary,aerobic organism—itisa‘single-bugdisease’.TB
peritonitiswillbediscussedelsewhere( Chapter38)
Tertiaryperitonitis
This entity does exist, yet it is impossible to define it in a couple of
sentences. No wonder your mind (and sometimes ours) is clouded by
confusion. One way to understand this syndrome is to list its most
commoncharacteristics:
•
ItoccursinICUpatientswithmulti-organdysfunction.
•
Itisthesequelofseveresecondaryperitonitis,typicallytreatedwith
multipleantibioticsandrepeatedabdominalexplorations.
•
Atsurgery,athin,cloudy,poorlywalled-offexudate is found in the
absenceofadefinitesourceofintra-abdominalinfection.
•
The microbial inoculum typical of tertiary peritonitis is unusual. In
some cases, highly pathogenic, antibiotic-resistant species (e.g.
PseudomonasorEnterobacter)areencountered.Inothers,theflora
is really weird, consisting mainly of organisms of normally low
pathogenicity such as Staphylococcus epidermidis, Enterococcus
andCandidaalbicans.Thisiswhythesepatientsarethoughttobe
immunocompromised. Are these organisms the cause of the
syndromeinahosttooweaktofightbackormeremarkersofa
deepermalaise?
Thissyndromeillustratestheparadoxofmodernmedicine.Ontheone
hand,itisanoutcomeofunsuccessful treatmentofaseveresecondary
peritonitis.Ontheotherhand,high-techinterventionshavepermittedthe
emergenceofthiscategoryofpatientswhowouldhavesuccumbedmuch
earlier to their disease only two or three decades ago (so, yes, a
measure of success). When peritonitis persists, despite adequate
source control and repeated reoperations, think about tertiary
peritonitis!
If a patient operated upon for secondary peritonitis has no evidence of anastomotic leak or
residualabscess,i.e.‘normal’CT,andisnotsmilingonday7—thinkabouttertiaryperitonitis!
Ari
Letuslookatareal-lifeexample:
A 75-year-old male undergoes an emergency subtotal colectomy with an ileorectal
anastomosisforanobstructingcarcinomaofthesigmoidcolon.Heisrushed,6dayslater,for
a relaparotomy because of diffuse peritonitis and a documented free anastomotic leak. At
operation,hisabdomenisfoundtobefulloffecalmaterial.Itiscleansedandtheanastomosis
isdismantled;therectumisclosedasinaHartmann’sprocedureandtheileumexteriorizedas
anend-ileostomy.Theabdomenisleftopenasa‘laparostomy’.Ataplannedrelaparotomy48
hourslater,residualcollectionsof‘thin’pusareevacuated.Thepatientcontinuestobe‘septic’
anddevelopsamulti-organdysfunctionsyndrome(MODS).ACTscanoftheabdomenshows
fluidinthepelvisandgutters;diagnosticaspirationrevealsthepresenceoffungi.Anantifungal
agentisaddedtothebroad-spectrumantibioticsthepatientisalreadyreceiving.Hecontinues
todeteriorate;at relaparotomy,murkyperitonealfluidisfound andcultured.ItgrowsCandida
andStaph.epidermidis, triggering yet again an antibiotic readjustment. The MODSworsens,
leadingtothepatient’sdemise5weeksafterthefirstoperation.Thehospitalbillamountstoa
staggering$250,000(itcouldbeamillioninanotherivorytower—asyouknowhospitalbilling
israndomanddoesn’tmakeanysense…).
Intertiaryperitonitis,further antimicrobialadministrationandoperative
interventions seem futile and may contribute to the peritoneal
superinfection and possibly to the aggravation of the SIRS-MODS
complex.Thefrequentlyfataloutcomeoftertiaryperitonitisindicatesthat
currentantibiotic-assisted,mechanicalanswerstosevereperitonitishave
aboutreachedtheirlimits,inan(atleastfornow)unsalvageablepatient.
Some surgeons find it difficulttoacceptfutilityandavoid surgery when
facedwithperitonitis,especiallysincesupportivecare,evenifsuccessful,
islongand frustrating,andthepressure“to dosomething”isstrong.Of
course,manygeneralsurgeonsnevercomeacrossthisentity:their
patienteitherdiesbeforereachingthisphaseoristransferredtoan
ivorytower…
Management(secondaryperitonitis)
The outcome of IAI depends on the patient’s pre-morbid reserves, his current
physiological compromise and the virulence of the infection. Your goal is to assist the
patient’sownlocalandsystemicdefenses.
The philosophy of management in a typical case of secondary
peritonitis consists of initial adjunctive measures, source control,
followed by peritoneal toilet. More aggressive methods will also be
discussed.
Adjunctivemeasures
These refer to the stabilization of a sick patient by means of
appropriatefluid and electrolyte replenishment. The invasiveness ofthe
monitoring should be tailored to the physiologic status of the patient.
Broadantibiotic coverage foraerobicand anaerobicgutflora should be
startedearly.Inperitonitis,operatingonapoorlyresuscitatedpatient
islikethrowingbothendsoftheropeatadrowningman.
Sourcecontrol
1
In some cases (e.g. acute uncomplicated diverticulitis or acute
cholecystitis), i.v. antibiotics suffice to effect source control, at least
initially.Inmostetiologiesofsecondaryperitonitis,thekeytosuccessis
timelysurgicalinterventiontointerruptthedeliveryofbacteriaand
adjuvantsofinflammation(bile,blood,fecalmatter,barium)intothe
peritonealcavity.Allothermeasuresarefutileiftheoperationdoesnot
successfullyeradicatetheinfectivesourceandreducetheinoculumtoan
amount that can be handled effectively by the patient’s defenses,
supported by antibiotic therapy. This component of treatment is
uncontroversial.Sourcecontrol frequentlyinvolvesasimpleprocedure
such as an appendectomy or a patch-closure of a perforated ulcer.
Occasionally,amajorresectiontoremovetheinfectivefocusisindicated,
suchasgastrectomyforperforatedgastriccarcinomaoracolectomyfor
perforated diverticulitis. Generally, the choice of the procedure (e.g.
stoma versus primary anastomosis), depends on the anatomical
source of infection, the degree of peritoneal inflammation, the
patient’s premorbid reserves and the degree of SIRS, as will be
discussedintheindividualchapters.
Notethatsituationsexistwhenthesourcecannotbe eradicated
ortheexpectedpricetopayforitsremovalisdeemedtoohigh.Less
radicaloptionsmaythenbeused,suchasdiversion(e.g.proximalstoma
inapatienttoounstabletotoleratearesection)ordrainage(e.g.leaking
duodenum).
Peritonealtoilet
Oncethesourceofinfectioniseradicated,cleaningtheperitoneal
cavity is aimed at minimizing the intraperitoneal bacterial load.
Severalmaneuversdeservediscussion:
•
Liquidcontaminantsandinfectedexudatesshouldbeaspiratedand
particulatematterremovedbyswabbingormoppingtheperitoneal
surfaces with moist laparotomy pads. Do it gently for the
peritonealsurfaceisyourfriend!
•
There is no scientific evidence that intra-operative peritoneal
lavage,cosmeticallyappealingandpopularwithsurgeonsasit
is, reduces mortality or infectious complications in patients
receiving adequate systemic antibiotics. Similarly, peritoneal
irrigation with antibiotics is not advantageous, and the addition of
antisepticsmayproducelocaltoxiceffects.Irrigatecopiously(touse
a term popular among American surgeons) if you wish but know
that, beyond wetting your own underwear and shoes, you will
probablynot accomplishmuch ( Figure13.1). Should you choose
to remain a dedicated irrigator, try to confine the irrigation to the
contaminatedarea — to avoidspreadings**t all around —anddo
remembertosuckoutallthelavagefluidbeforeyouclose;thereis
evidence that leaving irrigation fluids behind interferes with
peritoneal defenses by ‘diluting the macrophages’. Perhaps
bacteriaswimbetterthanmacrophages!
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