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Pancreatita acuta

Pancreatita acuta

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Jurnalul de Chirurgie, Iasi, 2005, Vol. 1, Nr. 1
[ISSN 1584 – 9341]
 
PANCREATITA ACUT
Ă
– FORMA SEVER 
Ă
 
Ioana Grigora
ş
 Clinica A.T.I. Spitalul “Sf. Spiridon” Ia
ş
iUniversitatea de Medicin
ă
 
ş
i Farmacie Ia
ş
i
 ACUTE PANCREATITIS - THE SEVERE FORM (Abstract):
Acute pancreatitis is an acute inflammatorydisease. Frequently it is a challenging condition for the surgeon and for the intensive care physician, taking into accountthat etiology is sometimes obscure, the pathophysiology is complex and incompletely understood, the timing of surgicaltreatment is still under debate and the general treatment is mostly supportive. The incidence is about 30 – 50 / 100.000 /year. In 80% of cases the disease is associated with interstitial edema, mild infiltration with inflammatory cells andintra- or peripancreatic fat necrosis. Evolution is benign and self-limited with proper treatment. The severe form occursless frequent (15 - 20%), results in long lasting hospitalization and is associated with high mortality (30 - 40%), due toinfected necrosis and multiple organ failure. Alcoholism and biliary disease account for 80% of cases. Rare etiologies of disease include metabolic factors (hypercalcemia, hyperlipoproteinemia, drug ingestion), obstructive factors (abdominaltumors, trauma, endoscopic retrograde cholecistopancreatography, and s.o.), infections (viral, parasitic) andhemodynamic factors. Postoperative pancreatitis is a complication after major abdominal surgery (abdominal aortaaneurism repair, extensive upper abdominal surgery, hepatic or cardiac transplant, so.). The common pathophysiological mechanism is pancreatic hypoperfusion. Acute pancreatitis is not a stable disease, beingcharacterized by time-dependent stages with specific morphologic and clinical patterns. The terminology used todesignate these stages is stated in the Ulm classification. Since the consensus Conference in Atlanta (1992) the severeform of acute pancreatitis is defined by the presence of organ dysfunction/failure or by the presence of localcomplications. The initiating event is the premature zymogene activation and the impairment of the exocytosis processwith local consequences (ongoing tissue necrosis) and general consequences (systemic inflammatory response). Theinflammatory response is locally perpetuated by hypovolemia and pancreatic and intestinal hypoperfusion. Thesystemic inflammatory response is present in severe acute pancreatitis and along with tissue hypoperfusion promotesthe development of multiple organ dysfunction/failure syndrome. The infection of the necrotic tissue occurs usually inthe third week of evolution and is caused by enteric bacteria. The intestine plays a major role in the pathophysiology of acute pancreatitis. Diagnosis includes positive diagnosis, assessment of etiology and assessment of severity. Severityscoring systems, biological markers and imaging techniques are used to assess severity. The most used severity scoringsystems are Ranson score, Imre score and Apache II score. TREATMENT: should be early instituted, aggressive,nonspecific, supportive and adapted to severity. Due to improvement in intensive care of severe forms, mortalitydecreased and the survival of fatal cases also increased (usual more than 3 weeks).CONCLUSIONS: In 80% of cases acute pancreatitis has a benign, self-limited evolution with favorable resultsof medical treatment. In 20% of cases systemic and/or local complication ensue – severe pancreatitis. Early recognitionof severe forms is the cornerstone of therapeutic success. The patient should be admitted to Intensive Care Unit for clinical, laboratory and imaging monitoring and treatment. Early and aggressive correction of hypovolemia andhemodynamic optimization are crucial for initial survival. Infection prevention and control are crucial for later survival.Supportive therapy is essential for prevention/treatment of multiple organ dysfunction/failure syndrome. The surgicaltreatment should be performed in well defined circumstances with proper timing. Despite research mortality is still high(30-40%) and increases to 80% in case of infected necrosis.KEYWORDS: SEVERE PANCREATITIS, APACHE II SCORE, RANSON SCORE, SURGICAL TREATMENT INPANCREATITISCorrespondence: Ioana Grigora
ş
, Clinica A.T.I. Spitalul “Sf. Spiridon” Ia
ş
i, B-dul Independentei, 1, Iasi 700111
INTRODUCERE
Pancreatita acut
ă
este o entitate patologic
ă
, ce pune numeroase probleme de diagnostic
ş
itratament. În forma ei sever 
ă
reprezint
ă
o adevarat
ă
provocare pentru medicul de terapie intensiv
ă
,c
ă
ci cauzele sunt multiple
ş
i uneori obscure, fiziopatologia complex
ă
 
ş
i incomplet descifrat
ă
,diagnosticul dificil, alegerea momentului optim al tratamentului chirurgical controversat
ă
, iar tratamentul este cel mai frecvent nespecific, de suport al diverselor sisteme
ş
i organe.Pancreatita acut
ă
are o inciden
ţă
de 30 - 50 cazuri/100.000 locuitori/an, incluzând toateformele [2]. 80% din cazuri au o evolu
ţ
ie benign
ă
, autolimitat
ă
. Din toate cazurile 15 - 20%evolueaz
ă
sever c
ă
tre forma necrotico-hemoragic
ă
[1-3], generând o mortalitate de 30 - 40% [3].Pacien
ţ
ii cu forme severe de pancreatit
ă
acut
ă
au spitaliz
ă
ri îndelungate (s
ă
 ptamâni sau luni) înTerapia Intensiv
ă
 
ş
i decesul este prin necroz
ă
pancreatic
ă
infectat
ă
 
ş
i insuficien
ţ
e pluriviscerale.
9
 
Jurnalul de Chirurgie, Iasi, 2005, Vol. 1, Nr. 1
[ISSN 1584 – 9341]
 
ETIOLOGIE
Pancreatita acut
ă
are numeroase cauze, cele mai frecvente fiind ingestia de alcool
ş
i litiaza biliar 
ă
, responsabile pentru aproximativ 80% din cazuri (tabelul I).
Tabelul I: Factori etiologici ai pancreatitei acute
factori metaboliciingestia de alcoolhipercalcemiadroguri (diuretice tiazidice, furosemid,acid etacrinic, tetraciclina, azatioprina,estrogenii, acid valproic etc.);Hiperlipidemiafactori mecanici obstructivilitiaza biliar 
ă
 obstruc
ţ
ia ansei aferenteobstruc
ţ
ia duodenal
ă
 tumori periampulareulcer duodenal pancreas divisumtraumatismul pancreatic (contuziaabdominal
ă
, pl
ă
gi abdominale penetrante, pancreatita postoperatorie, dup
ă
 colangiografia retrograd
ă
endoscopic
ă
)factori infectio
ş
i parotidita epidemic
ă
 infec
ţ
ia cu virus Coxackieinfec
ţ
ia cu Micoplasmaascaridioza
ş
i alte parazitozefactori idiopatici Familialhipoperfuzia pancreatic
ă
 factori vasculari periarterita nodoas
ă
 
ş
i alte colagenozefactori embolicist
ă
ri de debit cardiac sc
ă
zut
Indiferent de factorul cauzal, procesul fiziopatologic ce caracterizeaz
ă
pancreatita acut
ă
estecomun tuturor formelor: activarea
ş
i eliberarea enzimelor pancreatice cu r 
ă
sunet local (distruc
ţ
ietisular 
ă
evolutiv
ă
)
ş
i r 
ă
sunet general (r 
ă
spuns inflamator sistemic).O entitate patologic
ă
tot mai frecvent întâlnit
ă
în serviciile de Terapie Intensiv
ă
este pancreatita acut
ă
ce survine ca o complica
ţ
ie postoperatorie sau complica
ţ
ie a unei boli preexistentegrave. Cauzele pancreatitei acute – complica
ţ
ie sunt: interven
ţ
ii chirurgicale abdominale majore,tratamentul chirurgical al anevrismului de aort
ă
abdominal
ă
, transplantul renal, transplantul cardiac,transplantul hepatic, diverse forme de
ş
oc. În toate aceste situa
ţ
ii, numitorul comun patogenic estehipoperfuzia pancreatic
ă
.Recunoa
ş
terea hipoperfuziei pancreatice ca mecanism patogenic este important
ă
nu numai pentru pancreatita acut
ă
postoperatorie, ci în toate formele de pancreatit
ă
acut
ă
. Hipoperfuzia pancreatic
ă
joac
ă
un rol important în conversia formelor u
ş
oare, autolimitate de pancreatit
ă
acut
ă
 c
ă
tre formele severe, necrotico-hemoragice. Recunoa
ş
terea acestui element patogenic are un impactclinic major, direc
ţ
ionând terapia ini
ţ
ial
ă
c
ă
tre o viguroas
ă
corec
ţ
ie a perfuziei tisulare.
FORME CLINICE
Evolu
ţ
ia natural
ă
a pancreatitei acute include mai multe forme clinice, fiecare cu tr 
ă
s
ă
turispecifice (clinice, fiziopatologice, radiologice, biochimice
ş
i bacteriologice) necesitând tratamentadaptat. Formele clinice de pancreatit
ă
acut
ă
 
ş
i inciden
ţ
a lor sunt redate în tabelul II (clasificareaUlm, 1995).
Tabelul II: Clasificarea formelor clinice de pancreatit
ă
acut
ă
(clasificarea Ulm)
 pancreatita intersti
ţ
ial
ă
edematoas
ă
71% pancreatita necrotic
ă
 
necroz 
ă 
steril 
ă 
 necroz 
ă 
infectat 
ă 
 21%
68%32%
 abcesul pancreatic 3% pseudochistul de pancreas 6%10
 
Jurnalul de Chirurgie, Iasi, 2005, Vol. 1, Nr. 1
[ISSN 1584 – 9341]
 
Pancreatita edematoas
ă
se caracterizeaz
ă
prin edem intersti
ţ
ial
ş
i necroz
ă
a gr 
ă
simii intra-
ş
i peripancreatice. În majoritatea cazurilor este autolimitat
ă
 
ş
i are o evolu
ţ
ie benign
ă
cu tratamentconservator. Pancreatita necrotic
ă
se caracterizeaz
ă
prin zone focale sau difuze de
ţ
esut pancreaticdevitalizat
ş
i necroz
ă
extensiv
ă
a
ţ
esutului gras retroperitoneal. Hemoragia este prezent
ă
în gradevariate. Infec
ţ
ia necrozei apare în 30 - 70% din cazurile de pancreatit
ă
necrotic
ă
. Abcesul pancreaticapare ca o colec
ţ
ie purulent
ă
a lojei pancreatice, adesea cu fuzee. Elementul definitor este izolareade germeni din lichidul abcesului. Caracteristic abcesului este prezen
ţ
a de puroi lichid ce poate fidrenat, spre deosebire de necroza infectat
ă
în care nu a ap
ă
rut înca lichefierea
ţ
esuturilor.Pseudochistul de pancreas, localizat în sau în jurul pancreasului are perete inflamator care îlindividualizeaz
ă
fa
ţă
de
ţ
esuturile din jur. De obicei, pseudochistul este o complica
ţ
ie tardiv
ă
a pancreatitei necrotice cu necroz
ă
steril
ă
.Din 1992 exist
ă
un consens în ceea ce prive
ş
te definirea formelor grave de pancreatit
ă
acut
ă
 (tabelul III). Pancreatita acut
ă
sever 
ă
este definit
ă
de prezen
ţ
a insuficien
ţ
ei unui/mai multor organe/sisteme
ş
i/sau de prezen
ţ
a complica
ţ
iilor locale: necroza steril
ă
, necroza infectat
ă
, abcesul pancreatic sau pseudochistul de pancreas.
Tabelul III: Pancreatita acut
ă
– forma sever
ă
(conferin
ţ
a de consens Atlanta 1992)
Insuficien
ţ
a unui/mai multor organe
ş
i sistemeComplica
ţ
ii localenecroza steril
ă
 necroza infectat
ă
 abcesul pancreatic pseudochistul de pancreas
 
PANCREATIT
Ă
ACUT
Ă
Pancreatit
ă
acut
ă
 edematoas
ă
 Pancreatit
ă
acut
ă
 necrotic
ă
 Rezolu
ţ
ie f 
ă
ă
 complica
ţ
ii Necroz
ă
steril
ă
Necroz
ă
infectat
ă
Pseudochist de pancreasAbces pancreaticZilele 1-4Zilele 6-21S
ă
 pt. 4-7
Fig. 1: Evolu
ţ
ia temporal
ă
a pancreatitei acute (Berger, 1997)
Debut
EVOLU
Ţ
IA TEMPORAL
Ă
A PANCREATITEI ACUTE
Contrar opiniei clasice în care unele cazuri de pancreatit
ă
acut
ă
edematoas
ă
evolueaz
ă
 ulterior spre necroz
ă
, ast
ă
zi se consider 
ă
pancreatita acut
ă
edematoas
ă
 
ş
i pancreatita necrotic
ă
cadou
ă
entit
ăţ
i mutual exclusive. Folosirea precoce a CT a demonstrat prezen
ţ
a necrozei pancreaticeîn primele 3 zile de la debut.În s
ă
 pt
ă
mâna 2 - 3, pancreatita acut
ă
edematoas
ă
evolueaz
ă
spre rezolu
ţ
ie, în timp ce pancreatita necrotic
ă
evolueaz
ă
ca necroz
ă
steril
ă
sau infectat
ă
. Necroza steril
ă
poate evolua spre
11

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