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Coperta:

Arh. Sorin Nistor


Tehnoredactare:
Radu Moldovanu
Copyright Jurnalul de chirurgie, Iai, 2005-2013

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Jurnalul de Chirurgie (Iai), 2013, Vol. 9, Nr. 2

Jurnalul de chirurgie este o revist electronic, cu acces liber (Open


Access), se adreseaz tuturor specialitilor chirurgicale i are drept obiective
asigurarea unui mijloc de informare eficient i ncurajarea tinerilor medici i
cercettori de a-i publica rezultatele activitii clinice i de cercetare.
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Committee of Medical Journals Editors (http://www.icmje.org).
ncepnd cu 2012, Jurnalul de chirurgie apare ntr-un nou format, este patronat de Academia de tiine
Medicale i, alturi de revista Chirurgia, este agreat oficial de Societatea Romn de Chirurgie i utilizeaz
serviciile CrossRef (DOI) pentru indexarea articolelor.
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Eugen Trcoveanu
Fondator & Redactor ef executiv
Radu Moldovanu
Redactori
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Comitet editorial internaional


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Jurnalul de Chirurgie (Iai), 2013, Vol. 9, Nr. 2

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Formate acceptate:
Articole:
1. Takaori K, Raut V, Uemoto S. Clinical significance of liver ischaemia after pancreatic resection. Br J Surg. 2011; 99(4): 597-598.
2. Iancu D, Barto A, Mocanu L et al. Rolul stentrii preoperatorii n chirurgia cancerului de pancreas. Jurnalul de chirurgie (Iai). 2011;
7(2): 188-192.
3. Diaconescu S, Barbu O, Vascu B, Moscalu C, Aprodu G, Gavrilescu S. [Hepatic and pulmonary hydatic cyst in a child]. Jurnalul de
chirurgie (Iai). 2011; 7(2): 274-278.
Cri:
1. Whitehead WE, Schuster MM. Gastrointestinal Disorders. Behavioral and Physiological Basis for Treatment. Orlando: Academic Press;
1985. p. 213-220.
2. Moldovanu R, Filip V, Vlad N. Elemente de anatomie chirurgical. Ghid pentru examenul de specialitate. Iai : Editura Tehnopress ;
2010. P. 178-179.
Capitole n cri i tratate :
1. Meltzer PS, Kallioniemi A, Trent JM. Chromosome alterations in human solid tumors. In: Vogelstein B, Kinzler KW, editors. The genetic
basis of human cancer. New York: McGraw-Hill; 2002. p. 93-113.
2. Jecu A. Patologia chirurgical a apendicelui. In : Angelescu N, editor. Tratat de patologie chirurgical vol. II. Bucureti : Editura
Medical ; 2003. P. 1595-1614.
Materiale electronice :
1. Skandalakis JE, Colborn GL, Weidman TA et al. Skandalakis' Surgical Anatomy. New York: McGraw Hill; 2004. DVD.
2. Kelly JC. Salivary Bacteria Might Reveal Pancreatic Cancer. Medscape Medical News. 2011; [available from
http://www.medscape.com/viewarticle/751552]

Tabelele vor fi inserate pe o pagin separat i nu vor depi o pagin; titlul tabelului va fi numerotat cu cifre
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bibliografice; articole multimedia: Power Point 50 Mb i 50 slide-uri; fiiere video de maxim 5GB.

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Jurnalul de Chirurgie (Iai), 2013, Vol. 9, Nr. 2

Jurnalul de chirurgie (Iai) aprilie iunie 2013; vol. 9; nr. 2


CUPRINS
EDITORIAL
TRATAMENTUL CU INHIBITORI DE POMP DE PROTONI NTRE BENEFICII I RISCURI
Ctlina Mihai, Mihaela Dranga, M. Badea, Otilia Nedelciuc, Cristina Cijevschi Prelipcean
Jurnalul de chirurgie (Iai) 2013; 9(2): 107-111.
DOI: 10.7438/1584-9341-9-2-1.
ARTICOLE DE SINTEZ
NECESITATEA REVIZUIRII CLASIFICRII ATLANTA A PANCREATITEI ACUTE
V. Punescu
Jurnalul de chirurgie (Iai) 2013; 9(2): 113-126.
DOI: 10.7438/1584-9341-9-2-2.
CHIMIOTERAPIA HIPERTERMIC INTRAPERITONEAL (CHIP) ASOCIAT CITOREDUCIEI
TUMORALE N TRATAMENTUL CARCINOMATOZEI PERITONEALE DE ETIOLOGIE
COLORECTAL
I. Huanu, I. Radu, B. Filip, Mihaela Buna, Maria Gabriela Aniei, M. Deraco, V. Scripcariu
Jurnalul de chirurgie (Iai) 2013; 9(2): 127-136.
DOI: 10.7438/1584-9341-9-2-3.
STRATEGII TERAPEUTICE N CANCERUL ESOFAGIAN: ROLUL TRATAMENTULUI CHIRURGICAL
B. Filip
anu, I. Radu, Maria-Gabriela Aniei, V. Scripcariu
Jurnalul de chirurgie (Iai). 2013; 9(2): 137-148.
DOI: 10.7438/1584-9341-9-2-4.
ARTICOLE ORIGINALE
INTRAOPERATIVE DIFFICULTIES IN LAPAROSCOPIC CHOLECYSTECTOMY
S.K. Sahu , A. Agrawal, P.K. Sachan
Jurnalul de chirurgie (Iai). 2013; 9(2): 149-155.
DOI: 10.7438/1584-9341-9-2-5.
IS GASTROESOPHAGEAL REFLUX DISEASE INFLUENCED BY DUODENOGASTRIC REFLUX ?
Mihaela-Aura Mocanu
, T. Nicolae, Monica Dumitrescu
Jurnalul de chirurgie (Iai). 2013; 9(2): 157-160.
DOI: 10.7438/1584-9341-9-2-6.
COMPLICAIILE PRECOCE ALE CHIRURGIEI CATARACTEI
C. Constantin
Jurnalul de chirurgie (Iai). 2013; 9(2): 161-165.
DOI: 10.7438/1584-9341-9-2-7.
CAZURI CLINICE
TRATAMENTUL PE CALE LAPAROSCOPIC N HERNIA INGHINAL MULTIPL - PREZENTARE
DE CAZ
Lucica Timiescu
Jurnalul de chirurgie (Iai). 2013; 9(2): 167-171.
DOI: 10.7438/1584-9341-9-2-8.

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Jurnalul de Chirurgie (Iai), 2013, Vol. 9, Nr. 2

THYMOMA WITH LATERAL AND PARACARDIAC EVOLVEMENT


Oana-Raluca Lucaciu, P.V-H. Boianu, T. Hogea, Claudia Dorob, A-M. Boianu
Jurnalul de chirurgie (Iai). 2013; 9(2): 173-178.
DOI: 10.7438/1584-9341-9-2-9.
MIASTENIA GRAVIS POST-TIMECTOMIE
C. Mota
Jurnalul de chirurgie (Iai). 2013; 9(2): 179-184.
DOI: 10.7438/1584-9341-9-2-10.
A CASE OF PENILE ENTRAPMENT IN METAL RINGS TREATED BY ASPIRATION AND PUNCTURE
TECHNIQUE
S. Kumar, A. Gupta
Jurnalul de chirurgie (Iai). 2013; 9(2): 185-188.
DOI: 10.7438/1584-9341-9-2-11.
GIANT SUBMUCOSAL GASTRIC LIPOMA CASE REPORT
Maria-Gabriela Aniei
, Oana Simionescu, Nora Lefter, V. Scripcariu
Jurnalul de chirurgie (Iai). 2013; 9(2): 189-192.
DOI: 10.7438/1584-9341-9-2-12.

TEHNIC CHIRURGICAL / MULTIMEDIA


LAPAROSCOPIC TRANSABDOMINAL PRE-PERITONEAL (TAPP) PROCEDURE FOR GROIN
HERNIA. HOW TO DO IT FOR BETTER OUTCOMES
R. Moldovanu
Jurnalul de chirurgie (Iai). 2013; 9(2): 193-196.
DOI: 10.7438/1584-9341-9-2-13.

ARC PESTE TIMP


COMENTARIU LA ARTICOLUL
CONTRIBUTION LA TECHNIQUE DU PNEUMOTHORAX EXTRA-PLEURAL - 75 CAS OPRS
(C. Crpinian, M. Oncesco - Revista de Chirurgie 1940; 9-10/43: 671-679.)
N.M. Constantinescu
Jurnalul de chirurgie (Iai). 2013; 9(2): 197-202.
DOI: 10.7438/1584-9341-9-2-14.
NOUTI
EUROAMERICAN MULTISPECIALITY SUMMIT VI. Laparoscopy & Minimally Invasive Surgery
R. Moldovanu, C. Tiu
Jurnalul de chirurgie (Iai). 2013; 9(2): 203-204.
DOI: 10.7438/1584-9341-9-2-15.

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Jurnalul de Chirurgie (Iai), 2013, Vol. 9, Nr. 2

Jurnalul de chirurgie [Journal of Surgery] (Iai) April June 2013; vol. 9; no. 2
TABLE OF CONTENT
EDITORIAL
PROTON PUMP INHIBITORS BETWEEN BENEFITS AND RISKS
Ctlina Mihai, Mihaela Dranga, M. Badea, Otilia Nedelciuc, Cristina Cijevschi Prelipcean
Jurnalul de chirurgie (Iai) 2013; 9(2): 107-111.
DOI: 10.7438/1584-9341-9-2-1.
REVIEWS
NECESSITY TO REVIEW ATLANTA CLASSIFICATION OF ACUTE PANCREATITIS
V. Punescu
Jurnalul de chirurgie (Iai) 2013; 9(2): 113-126.
DOI: 10.7438/1584-9341-9-2-2.
HYPERTHERMIC INTRAPERITONEAL CHEMOTHERAPY WITH CYTOREDUCTIVE SURGERY FOR
THE TREATMENT OF PERITONEAL CARCINOMATOSIS FROM COLORECTAL ORGIN
I. Huanu, I. Radu, B. Filip, Mihaela Buna, Maria Gabriela Aniei, M. Deraco, V. Scripcariu
Jurnalul de chirurgie (Iai) 2013; 9(2): 127-136.
DOI: 10.7438/1584-9341-9-2-3.
THERAPEUTIC STRATEGIES IN OESOPHAGEAL CANCER:
TREATEMENT
B. Filip
anu, I. Radu, Maria-Gabriela Aniei, V. Scripcariu
Jurnalul de chirurgie (Iai). 2013; 9(2): 137-148.
DOI: 10.7438/1584-9341-9-2-4.

THE

PLACE

OF

SURGICAL

ORIGINAL ARTICLES
INTRAOPERATIVE DIFFICULTIES IN LAPAROSCOPIC CHOLECYSTECTOMY
S.K. Sahu , A. Agrawal, P.K. Sachan
Jurnalul de chirurgie (Iai). 2013; 9(2): 149-155.
DOI: 10.7438/1584-9341-9-2-5.
IS GASTROESOPHAGEAL REFLUX DISEASE INFLUENCED BY DUODENOGASTRIC REFLUX ?
Mihaela-Aura Mocanu
, T. Nicolae, Monica Dumitrescu
Jurnalul de chirurgie (Iai). 2013; 9(2): 157-160.
DOI: 10.7438/1584-9341-9-2-6.
EARLY COMPLICATIONS OF CATARACT SURGERY
C. Constantin
Jurnalul de chirurgie (Iai). 2013; 9(2): 161-165.
DOI: 10.7438/1584-9341-9-2-7.
CASE REPORT
LAPAROSCOPIC TREATMENT FOR MULTIPLE INGUINAL HERNIAS CASE REPORT
Lucica Timiescu
Jurnalul de chirurgie (Iai). 2013; 9(2): 167-171.
DOI: 10.7438/1584-9341-9-2-8.

vi
Jurnalul de Chirurgie (Iai), 2013, Vol. 9, Nr. 2

THYMOMA WITH LATERAL AND PARACARDIAC EVOLVEMENT


Oana-Raluca Lucaciu, P.V-H. Boianu, T. Hogea, Claudia Dorob, A-M. Boianu
Jurnalul de chirurgie (Iai). 2013; 9(2): 173-178.
DOI: 10.7438/1584-9341-9-2-9.
MIASTENIA GRAVIS AFTER THYMECTOMY
C. Mota
Jurnalul de chirurgie (Iai). 2013; 9(2): 179-184.
DOI: 10.7438/1584-9341-9-2-10.
A CASE OF PENILE ENTRAPMENT IN METAL RINGS TREATED BY ASPIRATION AND PUNCTURE
TECHNIQUE
S. Kumar, A. Gupta
Jurnalul de chirurgie (Iai). 2013; 9(2): 185-188.
DOI: 10.7438/1584-9341-9-2-11.
GIANT SUBMUCOSAL GASTRIC LIPOMA CASE REPORT
Maria-Gabriela Aniei
, A. Gervescu, Oana Simionescu, Nora Lefter, V. Scripcariu
Jurnalul de chirurgie (Iai). 2013; 9(2): 189-192.
DOI: 10.7438/1584-9341-9-2-12.

SURGICAL TECHNIQUE / MULTIMEDIA ARTICLE


LAPAROSCOPIC TRANSABDOMINAL PRE-PERITONEAL (TAPP) PROCEDURE FOR GROIN
HERNIA. HOW TO DO IT FOR BETTER OUTCOMES
R. Moldovanu
Jurnalul de chirurgie (Iai). 2013; 9(2): 193-196.
DOI: 10.7438/1584-9341-9-2-13.

ARCH BEYOND TIME


COMMENTS ABOUT THE PAPER
TECHNIQUE OF EXTRA-PLEURAL PNEUMOTHORAX 75 CASES
(C. Crpinian, M. Oncesco - Revista de Chirurgie 1940; 9-10/43: 671-679.)
N.M. Constantinescu
Jurnalul de chirurgie (Iai). 2013; 9(2): 197-202.
DOI: 10.7438/1584-9341-9-2-14.

NEWS
EUROAMERICAN MULTISPECIALITY SUMMIT VI. Laparoscopy & Minimally Invasive Surgery
R. Moldovanu, C. Tiu
Jurnalul de chirurgie (Iai). 2013; 9(2): 203-204.
DOI: 10.7438/1584-9341-9-2-15.

EDITORIAL

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Jurnalul de Chirurgie (Iai), 2013, Vol. 9, Nr. 2

TRATAMENTUL CU INHIBITORI DE POMP DE PROTONI


NTRE BENEFICII I RISCURI
Ctlina Mihai, Mihaela Dranga, M. Badea,
Otilia Nedelciuc, Cristina Cijevschi Prelipcean
Universitatea de Medicin i Farmacie Gr.T. Popa Iai
Institutul de Gastroenterologie i Hepatologie Iai, Spitalul Sf. Spiridon Iai
PROTON PUMP INHIBITORS BETWEEN BENEFITS AND RISKS (Abstract): Proton pump
inhibitors (PPI) have been widely used since 1989 because they are highly effective for acidrelated conditions. As a class, PPIs are among the safest of pharmacologic agents. In the last years
concerns have risen regarding potential of adverse events due to PPI use. These include cancer
risk (stomach and colorectal cancer), infection risk (pneumonia, Clostridium difficile associated
diarrhea, small intestinal bacterial overgrowth, spontaneous bacterial peritonitis, interstitial
nephritis), metabolic effects on bone density with osteoporotic fractures, alteration of absorption
of vitamins and minerals and the pharmacodynamic interaction with the metabolism of other
medications by the hepatic cytochrome P450 enzyme systems (e.g., clopidogrel). Almost the
entire evidence base regarding the safety of PPI therapy is composed of retrospective nonrandomized studies that demonstrate association but not causality and are limited by potential
confounding factors. There is no evidence to support any benefit of changing existing clinical
practice for preventing any of the potential adverse effects associated with PPI therapy. Therefore,
in patients with appropriate indications for PPI, we should avoid continuous and high-dose
therapy, considering on-demand therapy in suitable patients and step-down strategy.
KEY WORDS: PROTON PUMP INHIBITORS; PPI; GASTRIC CANCER; OSTEOPOROSIS;
CLOSTRIDIUM DIFFICILE; CLOPIDOGREL
SHORT TITLE: Proton pumps inhibitors: benefits & risks
Inhibitorii pomei de protoni: beneficii i riscuri
HOW TO CITE: Mihai C, Dranga M, Badea M, Nedelciuc O, Mihai C. [Proton pump inhibitors between benefits and
risks]. Jurnalul de chirurgie (Iai). 2013; 9(2): 107-111. DOI: 10.7438/1584-9341-9-2-1.

Inhibitorii pompei de protoni (IPP)


reprezint clasa de medicaie cu cea mai
larg prescriere n gastroenterologie.
Utilizai n practica clinic de peste 20 de ani
(din 1989), n S.U.A. se nregistreaz peste
100 milioane de reete anual, fiind
considerat a treia clas de medicamente ca
volum al vnzrilor [1]. IPP inactiveaz
ireversibil
H+ / K+ - ATP-aza
(pompa
protonic) la nivelul celulelor parietale
gastrice, determinnd scderea produciei
zilnice de acid clorhidric cu 80-95%.
Supresia acid se menine 24-48 de ore, pn
la sinteza de noi molecule de pomp
protonic.
Indicaiile administrrii de IPP sunt
variate i includ afeciuni frecvent ntlnite

n practica clinic curent: boala de reflux


gastro-esofagian, ulcerul gastric i duodenal,
gastritele, dispepsia funcional. Fac parte
din toate schemele de eradicare a infeciei cu
Helicobacter pylori, se asociaz la pacienii
aflai n tratament cu antiinflamatorii nonsteroidiene sau antiagregante plachetare. n
patologia chirurgical IPP sunt folosii n
tratamentul hemoragiei digestive superioare
non-variceale, ulcerului peptic complicat,
pancreatitei acute, precum i n prevenirea i
tratarea gastritei i ulcerului de stress la
pacienii aflai n stare critic.
Dintre IPP fac parte: omeprazolul,
pantoprazolul, esomeprazolul, lansoprazolul,
dexlansoprazolul i rabeprazolul, ultimii doi
nefiind disponibili n Romnia. Se pot

Adresa de coresponden: Prof. Dr. Cristina Cijevschi Prelipcean


Institutul de Gastroenterologie i Hepatologie Iai, Spitalul Sf. Spiridon, Iai
Bd. Independenei nr.1, 700111, Iai, Romnia
Tel. / Fax: 0040 (0) 232 26 75 00
E-mail: cristinacijevschi@yahoo.com

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Mihai C. et al.

Jurnalul de Chirurgie (Iai), 2013, Vol. 9, Nr. 2

administra per os sau intravenos, doza


uzual fiind de 40 mg/zi pentru omeprazol,
pantoprazol, esomeprazol i 30 mg/zi pentru
lansoprazol.
Considerate n general medicamente
sigure i eficace, administrarea lor nu este
ns lipsit de efecte secundare, care trebuie
cunoscute, prevenite i tratate corespunztor.
Dintre potenialele efecte secundare
ale IPP fac parte: riscul carcinogenetic
(cancer gastric, tumori carcinoide, cancer
colorectal), riscul infecios (pneumonie,
diaree acut, colit pseudomembranoas,
sindrom de suprapopulare bacterian a
intestinului subire, peritonit bacterian
spontan, nefrit interstiial), afectarea
metabolismului osos cu reducerea densitii
minerale osoase i creterea riscului de
fracturi, malabsorbia vitaminelor i
oligoelementelor, interaciunile cu alte
medicamente ce se metabolizeaz hepatic pe
calea citocromului P450 (cea mai studiat
asociere fiind ntre IPP i clopidogrel). Toate
aceste poteniale efecte secundare trebuie
privite ns cu reinere, att timp ct cele mai
multe au fost semnalate n urma unor studii
retrospective de tip caz-control. n lipsa
studiilor randomizate se poate demonstra
asocierea dar nu poate fi dovedit
cauzalitatea i nu pot fi eliminai factorii de
risc asociai consumului de IPP [2].
IPP i riscul carcinogenetic
IPP i cancerul gastric
Pe modele animale folosirea pe termen
lung a IPP duce la creterea concentraiei
plasmatice a gastrinei i aclorhidrie,
favoriznd carcinogeneza gastric, precum i
la proliferarea celulelor enterocromafine cu
creterea riscului de apariie a tumorilor
neuroendocrine. La om se constat creteri
moderate ale nivelului gastrinei i
chromograninei A, fr modificri de tip
displazic sau neoplazic.
n plus, IPP diminu inflamaia
asociat gastritei cu Helicobacter pylori
(considerat carcinogen de ordinul I pentru
cancerul gastric). Se consider n prezent c
IPP nu reprezint un factor de risc pentru

adenocarcinom sau tumorile neuroendocrine


gastrice [3].
IPP i cancerul colo-rectal
Gastrina seric poate stimula creterea
celulelor epiteliale normale i a celor
maligne de la nivelul colonului. Studiile pe
modele animale au demonstrat c
hipergastrinemia poate favoriza progresia
spre adenom precursor al cancerului colorectal. Acest lucru nu este relevant ns n
administrarea la subiecii umani, o metaanaliz recent publicat demonstrnd c nu
exist nici o asociere semnificativ ntre
utilizarea IPP i riscul de carcinogenez
colo-rectal [4].
IPP i patologia infecioas
Utilizarea IPP se poate nsoi de
creterea riscului de infecii, prind scderea
barierei acide gastrice protective.
Exist un risc moderat de pneumonie
(de 1,89 ori mai mare) att la pacienii tratai
n ambulator ct i la cei spitalizai. O metaanaliz ce a inclus 9 studii randomizate i
peste 120 000 de pacieni tratai cu IPP a
demonstrat c riscul de pneumonie este
redus la pacienii tratai pe termen lung, dar
crete n cazul administrrii unor doze mari
pe termen scurt [5].
De asemenea, crete riscul de apariie
al peritonitei bacteriene spontane la pacienii
cirotici (la acetia se prefer administrarea
de inhibitori ai receptorilor H2) i al nefritei
interstiiale acute [1].
Aclorhidria crete riscul infeciilor
enterice i diareei acute de cauz infecioas.
Atunci cnd nu este imperios necesar se
recomand oprirea administrrii de IPP n
cazul unei cltorii ntr-o zon endemic
pentru infecii enterale.
Se constat creterea frecvenei
sindromului de suprapopulare bacterian a
intestinului subire la consumatorii de IPP,
ceea ce explic simptome ca diareea i
meteorismul abdominal. Asocierea este
statistic
semnificativ
atunci
cnd
diagnosticul sindromului de suprapopulare
bacterian se face prin culturi de la nivelul

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aspiratului duodenal sau jejunal, nu i n


cazul utilizrii testelor respiratorii [6].
Un subiect controversat este asocierea
dintre IPP i infecia cu Clostridium difficile.
Cele mai multe studii demonstreaz o
asociere pozitiv. Reducerea aciditii
gastrice favorizeaz supravieuirea sporilor
Clostridium difficile i a toxinelor sale,
inhib funcia de aprare a organismului i
favorizeaz colonizarea tractului digestiv
superior cu germeni patogeni. Totui infecia
apare de obicei la pacienii care prezint i
ali factori de risc (vrstnici, tarai, consum
de antibiotice) asociai consumului de IPP.
Severitatea i complicaiile colitei pseudomembranoase nu sunt dependente de dozele
sau durata tratamentului cu IPP. n schimb,
consumul de IPP este factor de risc
pentru recurena infeciei cu Clostridium
difficile [7]. Ghidurile actuale privind
managementul infeciei cu Clostridium
dificile nu conin recomandri privind
oprirea tratamentului cu IPP n cazul
apariiei colitei pseudomembranoase [8,9].
IPP, osteoporoza i riscul de fracturi
n 2010 FDA atrgea atenia asupra
creterii riscului de osteoporoz i fracturi la
consumatorii
de
IPP.
Mecanismele
incriminate sunt: reducerea absorbiei
calciului prin scderea aciditii gastrice,
hiperparatiroidismul
secundar
hipergastrinemiei i alterarea enzimelor implicate
n remodelarea osoas (H+ / K+ - ATP-aza
osteoclastic).
Subiectul rmne controversat studiile
din literatur variind de la cele care nu
evideniaz nici o legtur pn la cele care
indic o cretere cu 35% a riscului de
fracturi [10,11]. Factorii asociai care cresc
riscul osteoporotic la pacienii aflai n
terapie cu IPP sunt: tratamentul de lung
durat (peste 1 an), dozele mari (peste 30
mg/zi), statusul postmenopauz la femei,
terapiile asociate (corticoterapia, antipsihotice, antiparkinsoniene, antidepresive),
consumul cronic de alcool, comorbiditile
(demena senil, infarctul miocardic, boli
care evolueaz cu alterarea mobilitii) [12].

Conform recomandrilor actuale nu se


justific suplimentarea cu calciu la pacienii
tratai cu IPP pentru prevenirea fracturilor i
dac indicaia terapeutic este corect
tratamentul antisecretor se continu chiar n
prezena osteoporozei [1].
IPP i malabsorbia
Aciditatea gastric este necesar
pentru absorbia fierului i eliberrii
vitaminei B12 din proteine. Dei pot fi
ntlnite anomalii ale tabloului hematologic
anemia este rar manifest clinic n absena
altei etiologii. Au fost raportate i cazuri de
hipomagneziemie la pacienii tratai cu IPP.
Nu se recomand testarea magneziului de
rutin, la toi pacienii, ci doar la cei cu
factori de risc (malabsorbie, insuficien
renal) [13]
IPP i interaciunile medicamentoase
Este cunoscut riscul hemoragic
gastroduodenal la pacienii aflai n
tratament cu antiinflamatorii nonsteroide
(AINS) i antiagregante plachetare. Att
aspirina ct i clopidogrelul cresc de 2-4 ori
riscul de hemoragie digestiv superioar, iar
asocierea Clopidogrel AINS crete acest
risc de 7,5 ori [14]. Asocierea IPP la aceti
pacieni scade semnificativ riscul hemoragic,
cu pn la 80-90%. n 2010 Colegiul
American de Cardiologie a propus un
algoritm de asociere a IPP la tratamentul
antiagregant cu tienopiridine. Fiecare pacient
trebuie evaluat din punct de vedere al
riscului hemoragiei digestive superioare.
Dac pacientul prezint istoric de ulcer sau
hemoragie digestiv n antecedente sau dac
ia concomitent tratament anticoagulant, cu
AINS sau corticosteroizi se vor administra
IPP.
Chiar n absena factorilor de risc
menionai, dac pacientul necesit terapie
cu dou antiagregante i este vrstnic (peste
60 de ani) sau consumator cronic de alcool
sau prezint simptome de tip reflux gastroesofagian sau dispepsie funcional, asocierea
IPP este de asemenea indicat [15].

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Pe de alt parte, IPP se metabolizeaz


pe calea citocromului P450, intrnd astfel n
competiie cu numeroase alte medicamente
care au aceeai cale de metabolizare.
Competiia la nivelul CYP 2C19 este
responsabil de scderea eficacitii
clopidogrelului atunci cnd este administrat
concomitent cu IPP, att FDA ct i EMEA
recomandnd evitarea acestei asocieri atunci
cnd nu este absolut necesar.
Metabolizarea difer de la un IPP la
altul:
omeprazolul
i
lansoprazolul
interacioneaz
cu
clopidogrelul
iar
omeprazolul, esomeprazolul i rabeprazolul
interacioneaz cu prasugrelul.
n mod practic, atunci cnd asociem
IPP la terapia antiagregant, vom evita
omeprazolul i esomeprazolul, prefernd
pantoprazolul. Acesta din urm se
metabolizeaz pe 2 ci, din care una
independent de citocromul P450 i n acest
fel interacioneaz limitat cu medicaia
antiagregant competitiv [16].
O situaie mai rar ntlnit n practica
clinic curent este tratamentul concomitent
cu metotrexat. IPP inhib o protein
(ABCG2) implicat n transportul i
metabolizarea metotrexatului, crescnd
astfel toxicitatea acestuia. La aceti pacieni
se prefer nlocuirea IPP cu inhibitori
H2 [17].
CONCLUZII
IPP sunt una din cele mai utilizate
medicaii, cu i fr prescripie medical,
att la pacieni spitalizai, ct i n
ambulator. i-au dovedit eficacitatea,
superioar altor tratamente antisecretorii, n
tratamentul a variate afeciuni: ulcerul
gastric i duodenal, boala de reflux gastroesofagian, dispepsia funcional, sindromul
Zollinger-Ellison, eradicarea infeciei cu
Helicobacter pylori, prevenirea hemoragiei
digestive superioare la pacienii aflai n
tratament cu antiagregante plachetare sau
AINS, precum i prevenirea/tratarea
ulcerului i gastritei de stress la pacienii
aflai n stare critic. Utilizarea lor nu este
ns lipsit de efecte secundare, dintre care
cele mai importante sunt creterea riscului

infecios (i n special a infeciei cu


Clostridium difficile), osteoporoza i riscul
de fracturi, precum i interaciunile
medicamentoase (n special cu medicaia
antiagregant plachetar). Nu exist n
prezent evidene care s susin aciuni de
prevenie a potenialelor efecte secundare ale
IPP (de ex. determinarea de rutin a
densitii
minerale
osoase
sau
a
magneziului). Din aceste motive se
recomand utilizarea judicioas a IPP n
practica clinic, cu monitorizare atent la
persoanele vrstnice i tarate, reducerea
dozelor, tratament discontinuu, recurgerea la
strategia top down, evitarea omeprozalului
n cazul tratamentului concomitent cu
clopidogrel. n ateptarea noilor molecule ce
vor inhiba aciditatea gastric - compui
potasici care vor neutraliza pompa de
protoni prin legare competitiv trebuie s
folosim corect IPP pentru ca beneficiile s
depeasc riscurile terapiei.
CONFLICT DE INTERESE
Autorii nu declar niciun conflict de
interese.

BIBLIOGRAFIE
1. Johnson DA, Oldfield EC. Reported side
effects and complications of long-term proton
pump inhibitor use: dissecting the evidence.
Clinical Gastroenterology and Hepatology.
2013; 11: 458-464.
2. Yang YX. PPI adverse events: fact vs fiction.
AGA Spring Postgraduate Course. 2013: 1-13.
3. Heidelbaugh JJ, Kim AH, Chang R, Walker PC.
Overutilization of proton-pump inhibitors:
what the clinician needs to know. Ther Adv
Gastroenterol. 2012: 5(4) 219-232.
4. Ahn JS, Park SM, Eom CS, et al. Use of Proton
Pump Inhibitor and risk of colorectal cancer: a
meta-analysis of observational studies. Korean
J Fam Med. 2012; 33: 272-279.
5. Giuliano C, Wilhelm SM, Kale-Pradham SM.
Are proton pump inhibitors associated with the
development
of
community-acquired
pneumonia? A meta-analysis. Expert Rev Clin
Pharmacol. 2012; 5(3): 337-344.
6. Lo WK, Chan WW. Proton pump inhibitor use
and the risk of small intestinal bacterial
overgrowth:
a
meta-analysis.
Clinical
Gastroenterology and Hepatology. 2013; 11:
483-490.

Inhibitorii pompei de protoni: beneficii i riscuri

111
Jurnalul de Chirurgie (Iai), 2013, Vol. 9, Nr. 2

7. Kim JW, Lee KL, Jeong JB, et al. Proton


pump inhibitors as a risk factor for recurrence
of Clostridium-difficile associated diarrhea.
World J Gastroenterol. 2010; 16(28): 35733577.
8. Janarthanan S, Dilah I, Adler DG, et al.
Clostridium difficile associated diarrhea and
proton pump inhibitor therapy: a metaanalysis. Am J Gastroenterol. 2012; 107:
1001-1010.
9. McCollum DL, Rodriguez JM. Detection,
treatment and prevention of Clostridium
difficile infection. Clin Gastroenterol Hepatol.
2012; 10: 581-592.
10. Khalili H, Huang SE, Jacobson BC, et al. Use
of proton pump inhibitors and risk of hip
fracture in relation to dietary and lifestyle
factors: a prospective cohort study. BMJ.
2012; 344: 1-13.
11. Sahara AI, El-Halabi MA, Ghaith OA, et al.
Proton pump inhibitors have no measurable
effect on calcium and bone metabolism in
healthy young males: A prospective matched
controlled study. Metabolism Clinical and
Experimental. 2013: 518-526.
12. Yu EW, Bauer SR, Bain PA. Proton pump
inhibitors and risk of fractures: a meta-analysis

of 11 international studies. Am J Med. 2011;


124(6): 519-526.
13. Hess MW, Hoenderop JG, Bindels RJ, et al.
Systematic review: hypomagnesaemia induced
by proton pump inhibition. Aliment Pharmacol
Ther. 2012; 36: 405-412.
14. Johnson DA. Concomitant use of PPIs and
antiplatelet therapy. Gastroenterol Hepatol.
2011; 7: 7-10.
15. Abraham NS, Hlatky MA, Antman EM, et al.
ACCF/ACG/AHA 2010 expert consensus
document on the concomitant use of proton
pump inhibitors and thienopyridines: a focused
update of the ACCF/ACG/AHA 2008 expert
consensus document on reducing the
gastrointestinal risks of antiplatelet therapy
and NSAID use. Am J Gastroenterol. 2010;
105(12): 2533-2549.
16. Dunn SP, Steinhubl SR, Bauer D, et al. Impact
of Proton Pump Inhibitor therapy on the
efficacy of clopidogrel in the CAPRIE and
CREDO trials. J Am Heart Assoc. 2013; 2(1):
1-11.
17. Bezabeh S, Mackey AC, Kluetz P, et al.
Accumulating evidence for a drug-drug
interaction between methotrexate and proton
pump inhibitors. Oncologist. 2012; 17: 550-554.

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ARTICOLE DE SINTEZ

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NECESITATEA REVIZUIRII CLASIFICRII ATLANTA


A PANCREATITEI ACUTE
V. Punescu
Clinica chirurgical, Spitalul Clinic de Urgen Bagdasar-Arseni, Bucureti
Universitatea de Medicin i Farmacie Carol Davila Bucureti
NECESSITY TO REVIEW ATLANTA CLASSIFICATION OF ACUTE PANCREATITIS
(Abstract): The universal credit of the acute pancreatitis description goes to Reginald Fitz Huber,
who in 1889 classified acute pancreatitis in: hemorrhagic, gangrenous and suppurative, following
surgical and autopsy findings. Over time were used different criteria for classification of acute
pancreatitis. Classification of acute pancreatitis in 1992 in Atlanta introduced a uniform system
for assessing clinical severity and various complications of the disease, widely accepted
classification. In this classification, acute pancreatitis is presented in two forms: mild and severe.
Mild pancreatitis is associated with minimal dysfunction of organs and, eventually, it heals.
Severe form is associated with organ failure and/or local complications, such as necrosis, abscess
and pseudocyst. The increase of knowledge of pathophysiology in acute pancreatitis, the
introduction of advanced diagnostic and treatment means showed that some definitions have
created confusion and made absolutely necessary the revision of Atlanta classification. The
review includes criteria for assessing the severity and description of local complications. The
revised classification of acute pancreatitis in 2012 identifies in the dynamic evolution of the
disease, early stage and late stage, and classifies severity as: mild, moderate and severe, based on
the presence or absence of multiple organ failure and local complications in the two forms of
acute pancreatitis: interstitial edematous pancreatitis and necrotizing pancreatitis. Local
complications are: acute peripancreatic fluid complications, pancreatic pseudocyst, acute necrotic
collections and wall formed necrosis. CONCLUSION: This review demonstrates that revised
Atlanta classification is an useful tool for the management of acute pancreatitis and will allow to
decrease the morbidity and mortality of severe pancreatitis.
KEY WORDS: ACUTE PANCREATITIS; ATLANTA CLASSIFICATION
SHORT TITLE: Pancreatita acut clasificarea Atlanta revizuit
Acute pancreatitis revised Atlanta classification
HOW TO CITE: Punescu V. [Necessity to review Atlanta classification of acute pancreatitis] Jurnalul de chirurgie (Iai).
2013; 9(2): 113-126. DOI: 10.7438/1584-9341-9-2-2.

Pancreatita acut este o boal


inflamatorie a pancreasului exocrin, care,
frecvent
intereseaz
i
esuturile
peripancreatice i sisteme de organe de la
distan, cu o patologie complex, cu o
evoluie adesea imprevizibil, cu consecine
dezastruoase, despre care Sir Berkeley
Moynihan spunea n articolul Acute
pancreatitis, publicat n Annals of Surgery,
n 1925 [1], c este cea mai teribil dintre
toate calamitile ce survin n legtur cu un
viscer abdominal. Debutul ei brusc, agonia
nelimitat care o acompaniaz i mortalitatea
ei crescut, toate mpreun o fac s fie cea

mai formidabil dintre catastrofe; George


Dieulafoy n Manuel de Pathologie Interne,
o numea drama pancreatic. Henri
Mondor, n Diagnostic urgents. Abdomen,
[31] o descrie ca o catastrof abdominal
caracterizat prin intensitatea semnelor
funcionale, precocitatea semnelor generale
i srcia relativ a semnelor fizice.
Mai recent, Lucien Leger, n articolul
Les pancreatites aigues, o descrie ca o
explozie ntr-o uzin de armament [5]
Creditul universal al descrierii
sistematice a pancreatitei acute i se acord
lui Reginald Huber Fitz (1843-1913), care a

Received date: 28.11.2012


Accepted date: 20.02.2013
Adresa de coresponden: Prof. Dr. Virgil Punescu
Str. Plutonier Petre Ionescu Nr. 12, Bloc 15, Scara A, etaj IV, Apartament 22, sector 3, Cod 032392, Bucureti
Tel.: 0040 (0) 724 39 58 53
E-mail: validor2004@yahoo.com

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Jurnalul de Chirurgie (Iai), 2013, Vol. 9, Nr. 2

corelat permanent informaiile clinice cu


cele chirurgicale i autopsice, i a publicat n
revista Boston Medical Surgical Journal din
21 februarie 1889, lucrarea Acute
Pancreatitis: A Consideration of Pancreatic
Hemorrhage, Hemorrhagic, Supurative and
Gangrenous Pancreatitis and Disseminated
Fat Necrosis, realiznd prima clasificare a
bolii n cele trei forme [5]. Lucrrile lui Fitz
au facilitat, n deceniile ulterioare, efectuarea
altor cercetri. n general, n sistemul de
clasificare, s-au folosit informaii provenite
din clinic, informaii chirurgicale sau
necropsice. Datorit prezentrii clinice
extrem de variate a bolii, n ciuda
cunotinelor avansate n nelegerea
fiziopatologiei
pancreatitei
acute,
a
tratamentului intensiv, boala prezint o mare
morbiditate i mortalitate.
Incidena pancreatitei acute este n
cretere pe plan mondial [6], i a fost de
43,8/100.000 locuitori n California, S.U.A.,
n 2001 [7] i de 45,3/100.000 locuitori n
Europa, n 2005 [8].
n S.U.A., numrul pacienilor
internai n spitale pentru pancreatit acut a
crescut de la 183.000 de cazuri n 1982, la
220.000 de cazuri n 2007 [9].
Mortalitatea general n pancreatita
acut variaz ntre 2 i 16%, n formele
uoare, iar n formele severe, nsoite de
insuficiene multiple ale sistemelor de
organe (Multiple Organ Failure - MOF),
atinge 30%, ca s ajung la 95% n necroza
pancreatic infectat [10].
Pentru diferenierea diverselor forme
morfopatologice i clinice ale pancreatitei
acute i pentru asigurarea unui tratament
individualizat, n clasificarea pancreatitei
acute s-au folosit diverse criterii clinice,
morfologice, biochimice, bacteriologice, sau
alte mijloace sofisticate de diagnostic ca:
tomografia computerizat, imaginile de
rezonan magnetic, colangiopancreatografia retrograd endoscopic, ultrasonografia.
Astfel, primul simpozion de la
Marsilia din 1963, mparte pancreatita acut
pe baza autopsiilor n dou forme: acut i
acut recurent [11]. S-a demonstrat rapid

c, dei clasificarea este simpl, n stadiul


precoce al bolii nu este posibil diferenierea
pancreatitei acute recurente de exacerbarea
acut a pancreatitei cronice.
La al doilea Simpozion de la Marsilia
din 1984 [12], definiia pancreatitei acute s-a
stabilit pe baza datelor chirurgicale i
necropsice [12]. Datele au fost completate la
Simpozionul de la Roma din 1988.
Simpozionul din 1984 de la Cambridge
clasific pancreatita acut n uoar i sever
n funcie de prezena complicaiilor.
Complicaiile identificate sunt: flegmonul,
pseudochistul,
abcesul,
necroza
i
hemoragia [13]. Definiiile s-au bazat pe
datele chirurgicale i necropsice. Pentru
clasificarea gradului leziunilor pancreatice
au fost folosite imaginile tehnice oferite de
ultrasonografie, de colangiopancreatografie
retrograd endoscopic i tomografia
computerizat. Noile metode de diagnostic
au permis o mai bun corelaie ntre gradul
modificrilor morfologice ale pancreasului i
intensitatea i frecvena complicaiilor
generale i locale [14], dar au continuat s
existe confuzii datorit definiiilor i
terminologiei folosite n descrierea i
diferenierea complicaiilor pancreatitei
acute [15]. Au continuat s fie propuse noi
clasificri bazate pe diverse criterii [16,17].
n septembrie 1992, 40 de experi n
pancreatita acut, anatomiti, gastroenterologi, interniti, patologi, radiologi i
chirurgi, reprezentnd 15 ri i ase
discipline medicale, dup trei zile de
dezbateri la Simpozionul Internaional de la
Atlanta, Georgia, S.U.A., au adoptat, prin
consens, definiiile despre pancreatita acut,
severitatea bolii, insuficiena multipl de
organe i complicaiile locale [18-20].
Clasificarea Atlanta ncearc s introduc
uniformitate n aprecierea severitii i a
diferitelor complicaii ale bolii. Conform
clasificrii Atlanta, pancreatita acut se
prezint sub dou forme: uoar i sever. n
aceast clasificare nu se folosete termenul
de pancreatit hemoragic, deoarece
hemoragia poate fi ntlnit i n afara
pancreatitei [16]. Pancreatita acut este
considerat a fi procesul inflamator al

Pancreatita acut clasificarea Atlanta revizuit

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pancreasului cu interesarea variabil a altor


esuturi regionale sau sisteme de organe
aflate la distan i se asociaz cu creterea
n snge i/sau urin a nivelului enzimelor
pancreatice.
Pancreatita acut uoar se asociaz cu
disfuncia minim a organelor i eventual se
vindec. Dup Societatea Britanic de
Gastroenterologie, prezena insuficienei
unui organ n prima sptmn i care se
rezolv n primele 48 ore, nu se consider un
indicator al atacului sever de pancreatit
acut [17]. Dac se efectueaz tomografie
computerizat parenchimul pancreatic este
normal. Din punct de vedere anatomopatologic, pancreatita acut uoar prezint
edem interstiial, chiar dac microscopic pot
fi identificate arii de necroz. Necroza
grsimii peripancreatice poate fi prezent
sau absent. Este important recunoaterea
ct mai precoce a formei uoare, deoarece
poate evolua rapid spre forma sever.
Pancreatita acut sever se asociaz cu
insuficiena organelor i/sau complicaiile
locale, reprezentate de coleciile lichidiene
acute, necroza, abcesul sau pseudochistul.
Pentru predicia severitii se folosete
scorul Ranson, egal sau mai mare de 3, sau
scorul APACHE, egal sau mai mare de 8.
Insuficiena organelor este definit
prin oc (presiunea sanguin sistolic mai
mic de 90 mmHg), insuficiena pulmonar
(presiunea parial a oxigenului, PaO2 sub 60
mmHg), insuficiena renal (creatinina peste
2 mg/dL sau peste 117 mol/L, dup
rehidratare), sngerare gastrointestinal
(peste
500
mL/24h),
coagulare
intravascular diseminat (trombocite sub
100.000/mm3, fibrinogen sub 1,0 g/L i
produii de degradare ai fibrinogenului peste
80 g/L) sau perturbri metabolice severe
(calciu sub 7,5 mg/dL sau sub 1,87 mmol/L).
Dintre complicaiile locale ce apar n
cursul pancreatitei acute severe, coleciile
lichidiene acute sunt localizate n pancreas
sau lng pancreas, fr perete de granulaie
sau esut fibros. Cele mai multe dintre
coleciile lichidiene acute regreseaz sau
evolueaz la pseudochist sau abces. Necroza
pancreatic, difuz sau localizat, prezint

parenchim pancreatic neviabil i este


asociat cu necroza peripancreatic.
Tomografia computerizat reprezint
testul gold standard n diagnosticul
necrozei. Focal sau difuz, nconjurat de
parenchim pancreatic normal, poate interesa
sub 30%, ntre 30 i 50% sau peste 50% din
pancreas. Necroza grsimii peripancreatice
poate fi superficial i n zone mici sau poate
fi profund i confluent. Hemoragia poate fi
prezent n pancreas i n esutul
peripancreatic. Microscopic, se constat
necroza extensiv a esutului gras interstiial,
lezarea vaselor i necroza celulelor acinare, a
celulelor insulelor pancreatice endocrine, a
sistemului canalelor pancreatice. Pentru
confirmarea necrozei pancreatice au fost
propui diveri markeri serici. Infecia
necrozei pancreatice crete gravitatea i
mortalitatea. Necroza pancreatic trebuie
difereniat de pseudochistul de pancreas i
de abcesul pancreatic.
Pseudochistul acut reprezint colecia
de suc pancreatic, bogat n enzime
pancreatice, care este nchistat de ctre un
perete fibros sau de esut de granulaie.
Formarea pseudochistului necesit patru
sptmni de la atacul acut al pancreatitei.
Frecvent, rmne steril.
Abcesul pancreatic este o colecie
circumscris de puroi, intraabdominal, de
obicei n jurul pancreasului, coninnd puin
sau nu esut necrotic pancreatic. Apare tardiv
n evoluia pancreatitei acute, mai trziu de
patru sptmni.
Stabilirea sistemului de clasificare a
pancreatitei
acute
la
Simpozionul
Internaional de la Atlanta din 1992 a oferit
un mijloc de ghidare clinic, universal
valabil
pentru
pancreatita
acut,
difereniind forma uoar de cea sever, fr
a se adresa aspectului dinamic al bolii.
Pentru recunoaterea formei severe se
folosesc criterii: clinice, evolutive, biologice,
imagistice, histologice.
Muli dintre termenii folosii n
clasificarea Atlanta, care descriu entitile
morfologice au fost interpretai diferit, mai
ales n descrierea coleciilor lichidiene
pancreatice i peripancreatice.

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O parte dintre definiii au creat


confuzii sau nu au fost acceptate, ori nu au
fost utilizate [23].
O mai bun nelegere a fiziopatologiei
pancreatitei acute [24-26], a insuficienei
multiple de organe [27-29], mbuntirea
diagnosticului
imagistic
[30-33],
i
dezvoltarea
mijloacelor
miniinvazive
radiologice [34], endoscopice [35], noile
tehnici de tratament operator a complicaiilor
[36,37] au fcut necesar revizuirea
Clasificrii Atlanta [28,38-40].
Propunerea de revizuire a Clasificrii
Atlanta se bazeaz pe conceptul c evoluia
natural a pancreatitei acute este bifazic,
prezentnd o faz precoce i o faz tardiv.
Aceast revizie include evaluarea severitii
clinice a pancreatitei acute i furnizarea mai
multor termeni obiectivi pentru descrierea
complicaiilor locale. Noul sistem de
clasificare acord atenie datelor de
morfologie, complicaiilor pancreatitei acute
i terminologiei. Pe msur ce cunotinele
despre patogenia i evoluia natural a bolii
s-au mbuntit, au aprut diferite definiii
i descrieri a diverse forme clinice de
pancreatit acut, unele greu de caracterizat,
iar folosirea de sinonime pentru unele forme,
ca abces pancreatic, flegmon pancreatic,
sau colecie pancreatic a creat confuzii i
a dus la Turnul Babel n pancreatit [39]
i au confirmat deficienele Clasificrii
Atlanta [23,28]. Clasificarea Atlanta
difereniaz forma uoara de cea sever,
fr a se adresa aspectului dinamic al bolii,
i, fr a distinge severitatea bolii ntre
prezena insuficienei multiple de organe i
complicaiile locale [40]. Pacienii care au
supravieuit atacului acut de pancreatit
acut, n lipsa unui terapii intensive energice
i susinute, dezvolt complicaii septice
datorit infectrii necrozei pancreatice sau
datorit altor procese septice [25].
Numeroase studii efectuate dup 1992 au
artat c n pancreatita acut sever, att
necroza pancreatic ct i insuficiena
multipl de organe, sunt factori semnificativi
de prognostic [29, 36, 41-43]. n insuficiena
multipl de organe mortalitatea variaz ntre
20 i 100%, n funcie de numrul organelor

interesate, severitatea insuficienei, durata i


tipul insuficienei, combinaia organelor
insuficiente [44,45]. n Clasificarea Atlanta a
pancreatitei acute severe nu se fcea
distincie ntre insuficiena funcional a
unui organ sau a mai multor organe, nici
dac insuficiena era tranzitorie sau
permanent [46]. n funcie de apariia
insuficienei multiple de organe, s-a propus
ca pancreatita acut sever s fie clasificat
n sever acut precoce i tardiv [47].
Forma
sever
acut
precoce
este
caracterizat prin dezvoltarea insuficienei
multiple de organe sau a sepsisului n
primele 72 de ore, prezent n 29,7% n
pancreatita necrotic, asociat cu o
mortalitate de 42% [47].
Durata n care se dezvolt pancreatita
acut sever precoce a fost extins la 7 zile
dup cum insuficiena multipl a organelor
apare n primele 72 de ore, n forma sever
fulminant; ntre 4 i 7 zile n forma sever
subfulminant; iar dac apare dup 7 zile,
sau mai trziu, s fie numit pancreatit
acut sever tardiv, grup n care
mortalitatea este sczut, 30,1% [48].
n raport cu evoluia dinamic a
pancreatitei acute severe i influenarea
prognosticului i a interveniilor terapeutice
specifice, s-a descris o form intermediar
de pancreatit acut sever, n care se
asociaz complicaiile locale, dar fr
persistena insuficienei funcionale a
organelor, form numit sever moderat
[40,49] (Tabel I).
n funcie de prezena sau absena
insuficienei de organe se propune ca
pancreatita acut sever s fie clasificat n
trei grupe:
1) grupa fr insuficiena organelor, n
care morbiditatea este mare, dar
mortalitatea intraspitaliceasc este
sczut sub 2%;
2) grupa n care exist un singur organ
insuficient;
3) grupa n care exist mai mult de dou
organe insuficiente, cu o mortalitate de
46% (exist o diferena statistic
semnificativ ntre aceste forme
P<0,01 [50]). Pacienii care prezint

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insuficiene multiple de organe


asociate complicaiilor infecioase
pancreatice i/sau peripancreatice, care
ating o mortalitate de 39%, se propune
a fi ncadrai n grupa pancreatite
acute severe [51].
n propunerile de revizuire a
Clasificrii Atlanta se consider c
pancreatita acut reflect variabilele

individuale ale pacientului [52] i se are n


vedere existena insuficienelor de organe,
dar i existena complicaiilor locale.
Insuficienele funcionale ale organelor
pot fi: absente, tranzitorii sau persistente,
iar complicaiile pancreatice i / sau
peripancreatice pot fi: solide, lichide sau
mixte, iar la rndul lor, pot fi sterile sau
infectate [51].

Tabelul I Clasificarea pancreatitei acute n funcie de criteriile de severitate


Pancreatita acut
Uoar

Complicaii locale

MOF

morbiditate

mortalitate

absente

absent

sczut

absent

PP

sau

tranzitorie

ridicat

sczut

Sever fulminant

PP+ infecioase

sau

foarte
crescut

foarte
crescut

Sever subfulminant

PP + infecioase

sau

crescut

crescut

Sever tardiv

PP + infecioase

sau

persist n primele 72
ore dup debut
persist dup 4-7 zile
de la debut
persist dup 7 zile de
la debut

crescut

sczut

Sever critic

PP + infecioase

persistent

crescut

excesiv

Moderat

MOF multiple organ failure (insuficiena multipl de organe) ; PP pancreatice sau/i peripancreatice

Evaluarea deficienelor Clasificrii


Atlanta [38-56] consemnate n literatura de
specialitate a fost prezentat n noiembrie
2006 la Chicago, Illinois, S.U.A., la
American
Pancreas
Association
i
International Association of Pancreatology,
care a analizat 447 articole, 12 ghiduri, care
se refereau la predicia pancreatitei acute i 8
reviste incluznd toate tipurile de publicaii
din perioada 1993-2006 [23,57]. Studiul a
analizat definiii ale Clasificrii Atlanta i a
evaluat interpretarea variat a acestor
definiii
referitoare
la
diagnosticul
pancreatitei acute, predicia severitii i a
criteriilor
de
severitate,
insuficiena
funcional a organelor i complicaiile
locale pancreatice i/sau peripancreatice.
Publicaiile
referitoare
la
revizuirea
criteriilor Atlanta au constituit un important
pas n viitor pentru The Acute Pancreatitis
Classifications Working Group. nc din
2007 [23,57] grupul de lucru a iniiat
revizuirea Clasificrii Atlanta, iar n 2012 a
oferit Consensul Internaional [58], publicat
n 2013 [59]. Consensul definete criteriile

pentru diagnosticul pancreatitei acute,


difereniaz cele dou forme ale pancreatitei
acute (pancreatita edematoas interstiial i
pancreatita necrotic), clasific severitatea
pancreatitei acute n trei categorii (uoar,
sever moderat i sever acut), definete
morfologia complicaiilor pancreatice i
peripancreatice ce apar n pancreatita acut.
Revizuirea intereseaz numai Clasificarea
Atlanta la adulii peste 18 ani i nu
intenioneaz s fie ghid terapeutic.
Consensul Internaional a fost obinut prin
ncorporarea rspunsurilor a 11 societi
naionale i internaionale ce studiaz
pancreasul.
Diagnosticul pancreatitei acute se
propune astfel, a fi stabilit pe baza a dou
din urmtoarele trei elemente:
1) durerea abdominal cu debut acut i
persistent, sever, localizat epigastric
i eventual iradiat n spate;
2) activitatea lipazelor sau activitatea
amilazelor serice s fie de trei ori mai
mare dect limita superioar a
normalului;

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3) caracteristicile pancreatitei acute s fie


gsite la tomografia computerizat
(Contrast
Enhanced
Computer
Tomography, CECT) i mai puin la
imaginile de rezonan magnetic
(MRI) sau la ecografia abdominal.
De precizat c dac diagnosticul este
stabilit pe durerea abdominal i creterea
activitii serice a amilazei sau lipazei,
diagnosticul bazat pe CECT nu este necesar
n camera de gard sau la internare.
Debutul pancreatitei acute este
considerat timpul cnd a nceput durerea
abdominal i nu timpul cnd a fost internat
n spital, dar trebuie nregistrat aceast
perioad de timp ca i datele dintre internare
i externare i transferul n alt serviciu sau n
alt spital.
n definirea tipurilor de pancreatit
acut se recunosc dou tipuri:
1) pancreatita edematoas interstiial i
2) pancreatita necrotic.
Pancreatita edematoas interstiial
este difuz, rar localizat, cu pancreasul
mrit datorit edemului. La CECT,
parenchimul pancreatic apare omogen mrit,
de
obicei
cu
inflamaia
grsimii
peripancreatice. Pot fi identificate colecii
lichide pancreatice i peripancreatice.
Simptomele
clinice
ale
pancreatitei
edematoase interstiiale se remit n mod
obinuit, n prima sptmn.
Pancreatita necrotic poate interesa
parenchimul pancreatic, esutul peripancreatic sau pe ambele i se dezvolt la
aproximativ 5-10% dintre pacieni. La
CECT, n primele zile ale bolii, zonele de
necroz sunt atenuate i se pot observa zone
mai puin demarcate sau confluente. n unele
cazuri, n prezena edemului interstiial,
poate exista necroza esutului peripancreatic,
crescnd morbiditatea. Evoluia necrozei
pancreatice i peripancreatice poate rmne
solid sau se lichefiaz, rmne steril sau se
infecteaz, persist sau dispare.
Pancreatita necrotic poate fi steril
sau infectat, fr corelaie ntre extensia
necrozei i riscul infeciei sau durata
simptomelor.

Infecia necrozei este rar n prima


sptmn de evoluie a bolii. Infecia poate
fi suspectat prin prezena la CECT a
gazelor n pancreas sau peripancreatic i
confirmat prin puncia ghidat cu ajutorul
CECT, cu ac fin (Fine-Needle Aspiration,
FNA), prin identificarea bacteriilor sau
ciupercilor. Cnd apare puroiul, supuraia
crete n acelai timp cu lichefierea.
Deoarece termenul de abces pancreatic din
Clasificarea Atlanta a creat confuzii, nu a
mai fost acceptat n noua clasificare.
Complicaiile pancreatitei acute se
refer la insuficiena organelor, la
complicaiile locale i la complicaiile
sistemice.
n noua clasificare, insuficiena se
refer
la
trei
organe:
respirator,
cardiovascular i
renal,
care
sunt
definite prin scorul Marshall modificat
(Tabelul II) [58].
Insuficiena organelor este definit
printr-un scor 2 sau mai mare pentru cel
puin unul dintre cele trei aparate (respirator,
renal sau cardiovascular). Pentru pacientul
din unitatea de terapie intensiv la care se
folosesc substane inotrope sau pentru
susinerea funciei respiratorii se folosete
scorul SOFA (Tabelul III) [60].
Complicaiile locale pot fi prezente sau
absente. Se descriu urmtoarele complicaii:
1) colecii lichidiene peripancreatice
acute;
2) pseudochistul pancreatic;
3) colecii necrotizante;
4) necroz cu perete format.
Alte complicaii locale ce pot fi
ntlnite: disfuncia evacurii gastrice,
tromboza venei splenice i a venei porte,
necroza colonului. Complicaiile locale pot
fi suspectate cnd persist sau reapare
durerea abdominal, secundar creterii
activitii enzimatice pancreatice serice,
creterii
disfunciei
organelor
sau/i
dezvoltrii semnelor clinice ale sepsisului,
ca febra i leucocitoza.
Coleciile
pancreatice
i
peripancreatice se descriu dup localizare:
pancreatice, peripancreatice i/sau dup tipul

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coninutului (lichid, solid, gaz) i grosimea


peretelui (subire, gros).
Complicaiile locale nu definesc
severitatea pancreatitei.
Complicaiile
sistemice
sunt
considerate exacerbrile comorbiditii
preexistente, cum ar fi: bolile arterelor

coronare,
bolile
pulmonare
cronice,
acutizarea pancreatitei. n clasificarea
revizuit se face distincie ntre persistena
insuficienei organelor, care definete
pancreatita acut sever i alte complicaii
sistemice reprezentate de exacerbarea
comorbiditii preexistente.

Tabelul II Scorul Marshall modificat pentru insuficiena multipl de organ (Multiple Organ Failure, MOF) [58]
Aparatul

Scor*
0

> 400

301 - 400

201 - 300

101 - 200

101

Creatinin seric (mol/L)

134

134 - 189

170 - 310

311 - 439

> 439

Creatinin seric (mg/dL)

< 1,4

1,4 - 1,8

1,9 - 3,6

3,6 - 4,9

> 4,9

> 90

< 90
Rspunde la
lichide

< 90
Nu rspunde
la lichide

< 90
Ph < 7,3

< 90
Ph < 7,2

Respirator (PaO2/FiO2)**
Renal***

Cardiovascular (TAS, mmHg)****

* scor 2, definete prezena insuficienei multiple de organe


** la pacientul neventilat FiO2 poate fi estimat astfel:
suplimentare respiratorie cu aer FiO2: 21%; suplimentare cu oxigen 2 L/min FiO2: 25%; suplimentare cu oxigen 4 L/min FiO2: 30%;
suplimentare cu oxigen 6-8 L/min FiO2: 40%; suplimentare cu oxigen 9-10 L/min FiO2: 50%.
*** la pacientul cu insuficien renal preexistent, orice deteriorare se corecteaz la valoarea creatininemiei 134 mol/L sau 1,4 mg/dL;
**** fr suport inotrop; TAS: tensiunea arterial sistolic

Tabelul III Scorul SOFA (SOFA (Sepsis-related Organ Failure Assessment) [60]
Scor* SOFA
Aparat respirator
PaO2 / FiO2
Coagulare
Trombocite (103/mm3)
Funcie hepatic
Bilirubina ( mol/L)
Aparat cardiovascular
Hipotensiune
Sistem nervos central
Glasgow Coma Scale
Funcie renal
Creatinina ( mol/L)
sau Diureza(mL/zi)

> 400

400

300

200**

100**

> 150

150

100

50

20

< 20

20 - 32

33 - 101

102 - 204

> 204

absence

< 70 mmHg***

Dopa
sau Dobutrex

Dopa > 5
sau Adren 0,1
sau Noradr 0,1

Dopa > 15
sau Adren > 0,1
sau Noradr > 0,1

15

13 - 14

10 - 12

6-9

<6

< 110

110 - 170

171 - 299

300 440
sau diureza < 500

> 440
sau diureza < 200

* scorul SOFA se calculeaz prin suma scorurilor fiecrui organ ; un scor mai mic ca 9 estimeaz o mortalitate de 33% n timp de un scor de
peste 11 estimeaz o mortalitate de 95% ;
** ventilaie mecanic ;
*** tensiune arterial medie ;
Dopa : Dopamina, g/kg/min ; Adren : Adrenalin, g/kg/min ; Noradr : Noradrenalin, g/kg/min

Evoluia pancreatitei acute cunoate


dou faze, care prezint dou vrfuri ale
mortalitii: precoce i tardiv.
Faza precoce, obinuit pn la sfritul
primei sptmni, este urmat de faza
secundar, tardiv, dup o sptmn pn la

o lun, pancreatita acut fiind o boal cu


evoluie dinamic.
Faza precoce rezult din rspunsul la
leziunea pancreatic local. Faza precoce
ocup obinuit prima sptmn, dar se
poate extinde i n a doua sptmn.

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Cascada citokinelor, activat de inflamaia


pancreatic, se manifest clinic sub forma
sindromului rspunsului inflamator sistemic
(Systemic
Inflammatory
Response
Syndrome, SIRS). SIRS este definit prin
prezena a dou sau mai multe din
urmtoarele criterii:
1) frecvena cardiac mai mare de 90 de
bti pe minut;
2) temperatura corpului sub 36C sau
peste 38C;
3) numrul celulelor albe sanguine sub
4000/mm3 sau peste 12000/mm3;
4) frecvena respiraiei peste 20/min sau
PCO2 sub 32 mmHg.
Persistena
SIRS
crete
riscul
dezvoltrii insuficienei organelor. Factorul
determinant al severitii pancreatitei acute
n faza precoce este reprezentat de prezena
i durata insuficienei organelor. Insuficiena
organelor poate fi tranzitorie, dac se
rezolv n 48 de ore, sau poate fi
persistent, dac insuficiena organelor
persist peste 48 de ore. Dac insuficiena
intereseaz mai mult de un organ, se
numete insuficien multipl a organelor
(Multiple Organ Failure, MOF). n faza
precoce pot fi identificate complicaii locale,
dar ele nu determin severitatea i pot
determina extensia necrozei. Modificrile
morfologice nu sunt proporionale cu
severitatea insuficienei organelor. n faza
precoce, pancreatita acut sever sau
moderat depinde de prezena i durata
insuficienei de organe.
Faza tardiv se caracterizeaz prin
persistena semnelor inflamaiei sistemice
sau prin prezena complicaiilor locale i
definete faza tardiv n pancreatita acut
sever moderat sau sever. n faza tardiv,
complicaiile locale evolueaz i au
implicaii
n
tratament.
Persistena
insuficienei organelor determin severitatea
pancreatitei acute n faza tardiv. Prezena
SIRS din faza precoce poate fi urmat de
rspunsul antiinflamator (Compensatory
Anti-inflammatory Response Syndrome,
CARS), care contribuie la creterea riscului
infeciei. Severitatea pancreatitei acute
trebuie identificat la internare, deoarece

pancreatita acut sever necesit tratament


precoce agresiv, i posibilitatea internrii n
servicii de specialitate.
n pancreatita acut sunt identificate
trei grade de severitate: uoar, moderat i
sever. Terminologia include insuficiena
organelor, care poate fi tranzitorie sau
persistent, i complicaiile locale i
sistemice.
Pancreatita
acut
uoar
se
caracterizeaz prin absena insuficienei de
organe i absena complicaiilor locale sau a
complicaiilor sistemice. Din punct de
vedere morfologic reprezint inflamaia
acut a parenchimului pancreatic i a
esuturilor peripancreatice, fr a recunoate
existena necrozei. Pancreatita edematoas
interstiial face ca parenchimul pancreatic
s apar mrit la CECT. Pacienii cu
pancreatit acut uoar sunt externai de
obicei n faza precoce a bolii. n mod
obinuit nu necesit investigaii tomografice,
iar mortalitatea este rar n aceast form.
Pancreatita acut sever moderat se
caracterizeaz prin prezena tranzitorie a
insuficienei organelor sau prin existena
complicaiilor locale sau a complicaiilor
sistemice, dar, n absena persistenei
insuficienei organelor. Aceast form a
pancreatitei acute se rezolv, n mod
obinuit, fr intervenie, sau evoluia se
poate prelungi n prezena necrozei sterile
extensive, dar fr insuficiena organelor. n
pancreatita
acut
sever
moderat,
mortalitatea este moderat, dar mai mic
dect n pancreatita acut sever.
Pancreatita
acut
sever
se
caracterizeaz prin existena insuficienei
organelor. Insuficiena organelor se poate
dezvolta n faza precoce a pancreatitei acute
prin activarea citokinelor, din care rezult
SIRS. Cnd SIRS este prezent i persist
crete riscul ca pancreatita s se complice
prin persistena insuficienei organelor i
impune ca pacientul s fie tratat ca avnd
pancreatit acut sever. Persistena
insuficienei unui organ sau a mai multor
organe crete riscul complicaiilor locale.
Persistena insuficienelor organelor n
primele zile ale bolii crete riscul deceselor,

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mortalitatea putnd ajunge la 50%. Infecia


necrozei la pacienii la care persist
insuficiena organelor se asociaz cu
mortalitate extrem de ridicat.
Evoluia severitii pancreatitei acute
este dificil de determinat dac insuficiena
organelor este prezent n primele 24 de ore,
deoarece nu se tie dac pacientul are o
insuficien tranzitorie a organelor sau una
persistent, dar va fi clasificat ca avnd
pancreatit acut sever. Dac insuficiena
organelor se rezolv dup 48 de ore va fi
clasificat ca avnd pancreatit acut sever
moderat, iar dac persist insuficiena
organelor va fi ncadrat ca avnd pancreatit
acut sever. Dup admiterea n spital,
pacientul va fi reevaluat dup 24 de ore, 48
de ore i 7 zile.
Dac n faza precoce se identific
existena complicaiilor locale, se vor
efectua investigaii pentru identificarea
modificrilor morfologice, deoarece:
1) prezena
i
extensia
necrozei
pancreatice i peripancreatice nu poate
fi definit n primele zile, necesitnd
repetarea CECT dup 5-7 zile;
2) extensia morfologiei i a necrozei nu
sunt direct proporionale cu severitatea
insuficienei organelor;
3) dac imaginile identific prezena
coleciilor lichidiene peripancreatice
sau a necrozei pancreatice, n general
ele nu sunt tratate n acest interval de
timp.
n faza tardiv a pancreatitei sever
moderate sau a pancreatitei acute severe,
complicaiile locale evolueaz, unii pacieni
cu persistena insuficienei organelor se pot
vindeca fr complicaii locale. Prezena
infeciei n zona de necroz crete riscul
deceselor. Infecia necrozei fr persistena
insuficienei organelor are o mortalitate mai
mic dect necroza infectat cu persistena
insuficienei organelor.
Diferenierea
morfologic
a
complicaiilor locale este necesar pentru
stabilirea tipurilor de intervenie. Descrierea
complicaiilor locale, care pot fi absente,
sterile sau infectate, i persistena
insuficienei organelor, a unui singur organ

sau a mai multor organe, trebuie precizat


fiindc tratamentul se adreseaz fiecrui caz.
Coleciile
pancreatice
i
peripancreatice se difereniaz dup coninutul
lichid sau solid. Sunt descrise urmtoarele
forme:
1) colecii lichidiene peripancreatice
acute, survenite n pancreatitele
edematoase interstiiale;
2) pseudochistul pancreatic, complicaie a
pancreatitei edematoase interstiiale, ce
apare n mod obinuit dup 4
sptmni;
3) coleciile necrotice acute din fazele
precoce ale pancreatitei;
4) necroza cu perete format, rar
dezvoltat nainte de 4 sptmni, i n
care peretele format este confirmat
radiologic.
Criteriile morfologice ale pancreatitei
acute, definite pe baza tomografiei
computerizate, combinate cu parametrii
clinici, ajut la instituirea tratamentului.
Pentru caracterizarea pancreatitei acute, cele
mai frecvente metode folosite pentru
identificarea modificrilor morfologice sunt
ultrasonografia
transabdominal
i
tomografia computerizat, la care se pot
aduga imaginile de rezonan magnetic
sau ultrasonografia endoscopic.
Colecia lichidian peripancreatic
acut se dezvolt n faza precoce a
pancreatitei acute edematoase interstiiale i
nu se asociaz cu necroza pancreatic.
Investigaiile imagistice nu identific un
perete format, colecia este omogen i, pot
fi prezente mai multe colecii. n majoritatea
cazurilor coleciile rmn sterile i se
rezolv spontan. Cnd colecia persist peste
4 sptmni se dezvolt pseudochistul
pancreatic.
Colecia
lichidian
peripancreatic acut se rezolv sau rmne
asimptomatic i nu necesit tratament i nu
se ncadreaz n pancreatita acut sever.
Pseudochistul pancreatic reprezint o
colecie lichidian peripancreatic, i, uneori
intrapancreatic, bine circumscris, rotund
sau oval, cu perei bine formai. Conine
material solid. De obicei prezint activitate
amilazic crescut, datorit rupturii canalului

Punescu V.

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Jurnalul de Chirurgie (Iai), 2013, Vol. 9, Nr. 2

pancreatic necrozat sau a ramurilor


intrapancreatice n parenchimul pancreatic
necrozat. Colecia apare dup 4 sptmni de
evoluie a pancreatitei acute edematoase
interstiiale. La tomografie computerizat
are
densitate
de
fluid
omogen,

cu perete bine definit, inflamator, complet


ncapsulat.
Metodele
imagistice
confirm
pseudochistul,
iar
ultrasonografia
i
imaginile de rezonan magnetic confirm
absena n colecie a materialului solid.

Tabelul IV Comparaie ntre clasificrile pancreatitei acute


Clasificarea Atlanta (1992)

Clasificarea Atlanta revizuit (2012)


Forme de pancreatit

Pancreatit acut uoar

Pancreatita acut edematoas intestiial

Pancreatit acut sever

Pancreatita acut necrotic


Predicia severitii

Insuficiena multipl de organ


oc (TAS < 90 mmHg)

Insuficiena multipl de organ


Absent sau
prezent cnd scor Marshall (sau SOFA*) 2
Cand este prezent poate fi tranzitorie sau persistent

Insuficien respiratorie (PaO2 60 mmHg)


Insuficien renal (creatinemie 177 mol/L sau 2
mg/dL dup rehidratare)
Hemoragie digestiv ( 500 mL/24h)
Coagulare intravascular diseminat
(trombocite 100000/mm3; fibrinogen < 1 g/L; sau
PDF 80g/L)
Perturbri metabolice
(calciu 1,87 mmol/L sau 7,5 mg/dL)
Scoruri de severitate
(Ranson > 3; APACHE II > 8)
Leziuni confirmate CT
Pancreatit edematoas

Abces pancreatic

Pancreatit interstiial edematoas


Colecii lichidene peripancreatice acute (acute
peripancreatic fluid collection)
Necroz pancreatic, colecie necrotic acut (acute
necrotic collection, ANC) sau necroz cu perete
format (walled-off necrosis, WON)
ANC, WON

Pseudochist pancreatic

Pseudochist pancreatic

Colecie lichidian acut


Necroz pancreatic

SIRS; MOF

Faze evolutive
Faz precoce:
rspunsul gazdei la leziunea pancreatic SIRS, MOF
Faza tardiv:
persistena SIRS i prezena complicaiilor locale
Clasificarea severitii
Pancreatita acut uoar

Disfuncie minim a unui organ


Evoluie spre vindecare
Pancreatita acut sever
Prezena MOF +/- complicaii locale

Absena MOF i a complicaiilor locale


Pancreatita acut sever moderat
MOF se remite n 48 h
Complicaii locale fr MOF
Pancreatita acut sever
Persistena MOF peste 48 h +/- complicaii locale

* prezena suportului inotrop sau a ventilaiei mecanice

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Colecia necrotic acut se dezvolt


dup 4 sptmni i conine lichid i esut
necrotic. Necroza se dezvolt n parenchimul
pancreatic i/sau n esutul peripancreatic. Se
poate asocia cu ruptura canalului pancreatic
n zona de necroz a parenchimului i se
poate infecta. n prima sptmn de
evoluie a bolii se difereniaz dificil colecia
lichidian acut, dar dup patru sptmni
diferena este clar, deoarece se asociaz
necroza
parenchimului
pancreatic,
confirmat de investigaiile imagistice sau
ultrasonografice, care nu evideniaz perete
definitiv de incapsulare.
Necroza cu perete format, perete
inflamator, apare dup patru sptmni de
evoluie a pancreatitei acute necrotice i
rezult din parenchimul pancreatic necrozat
i/sau din esutul peripancreatic necrozat.
Infecia necrozei poate fi i la distan de
pancreas.
Pentru
diferenierea
de
pseudochistul de pancreas se recurge la
imaginile de rezonan magnetic, la
ultrasonografia
transabdominal
sau
ultrasonografia endoscopic.
Necroza infectat este suspectat cnd
n colecia confirmat prin tomografie
computerizat se identific prezena gazului
n aria de necroz. Prezena gazului n aria
de necroz depinde de stadiul evolutiv al
bolii. n caz de dubiu, puncia cu ac fin
permite aspiraia pentru efectuarea culturilor
pentru germenii microbieni sau a fungilor.
Acurateea tomografiei computerizate
n predicia necrozei n fazele precoce, n
primele trei zile de la debutul simptomelor
pancreatitei
acute
severe
nu
este
satisfctoare [61,62]. Aria de necroz
depinde de fluxul sanguin pancreatic, care
scade n parenchimul pancreatic. Tomografia
computerizat efectuat n stadiile precoce
ale pancreatitei acute i care folosete
perfuzia substanei de contrast, identific
zonele n care fluxul sanguin este sczut
datorit
vasospasmului
arteriolar
intrapancreatic. Prin aceast metod [63,64]
se evalueaz circulaia sistemic anormal n
faza precoce a pancreatitei acute severe,
asigurnd un diagnostic mult mai precis al
necrozei pancreatice i se identific nc din

stadiile iniiale complicaiile locale i


sistemice. n funcie de prezena sau absena
necrozei, coleciile acute din primele patru
sptmni se numesc colecii lichidiene
peripancreatice acute sau colecii necrotice
acute. Din momentul dezvoltrii capsulei,
persistena coleciilor peripancreatice acute
se refer la pseudochist i la colecia
necrotic acut sau la necroza cu perete
format. Toate aceste colecii pot fi sterile sau
infectate.
Abandonarea vechilor termeni, ca
abces
pancreatic
sau
pseudochist
intrapancreatic
i
adoptarea
unei
terminologii standardizate propus de
clasificarea revizuit a pancreatitei acute, va
permite radiologilor, gastroenterologilor,
patologilor i chirurgilor aplicarea unui
tratament corect i o mai precis comparare
a rezultatelor cercetrilor efectuate n diverse
specialiti (Tabelul IV).
CONCLUZII
Lucrarea demonstreaz c clasificarea
Atlanta revizuit se constituie ntr-un util
instrument de lucru pentru managementul
pancreatitei acute, n vederea scderii
morbiditii i mortalitii pancreatitelor
acute severe.
CONFLICT DE INTERESE
Autorul nu declar nici un conflict de
interese.

BIBLIOGRAFIE
1. Moynihan B. Acute pancreatitis. Ann Surg.
1925; 81(1): 132-142.
2. Dieulafoy G. Pancratite aigue. Manuel de
Pathologie Interne, 16me edition, tome XII;
Paris: Masson et Cie; 1911. p. 66-67.
3. Mondor H. Pancratite aigue. Diagnostic
urgents. Abdomen, 9me edition; Paris:
Masson et Cie; 1965.
4. Leger L. Les pancreatites aigues. La Nouvelle
Presse Medicale. 1981; 10(32): 2575.
5. Fitz RH. Pancreatitis: a consideration of
pancreatic
hemorrhage,
hemorrhagic,
supurative and gangrenous pancreatitis and
disseminated fat necrosis. Boston Medical
Surgical Journal. 1889; 120(8): 181-187, 205207, 229-235.

124

Punescu V.

Jurnalul de Chirurgie (Iai), 2013, Vol. 9, Nr. 2

6. Talukdar R, Vege SS. Recent developments in


acute pancreatitis. Clin Gastroenterol.
Hepatol. 2009; 7(suppl. 11): S3-S9.
7. Frey CF, Zhou H, Harvey DJ, White RH. The
incidence and case-fatality rates of acute
biliary, alcoholic, and idiopathic pancreatitis in
California 1994-2001. Pancreas. 2006; 33(4):
336-344.
8. Yadav D, Lowenfels AB. Trends in the
epidemiology of the first attack of acute
pancreatitis: a systematic review. Pancreas.
2006; 33(4): 323-330.
9. Lowenfels AB, Maisonneuve P, Sullivan T.
The changing character of acute pancreatitis:
epidemiology, etiology and prognosis. Curr
Gastroenterol Rep. 2009; 11(2): 97-103.
10. Lankisch PG, Breuer N, Bruns A, WeberDany B, Lowenfels AB, Maisonneuve P.
Natural history of acute pancreatitis: a long term population based study. Am J
Gastroenterol. 2009; 104(11): 2797-2805.
11. Sarles H. Proposal adopted unanimously by
the participants of the symposium on
pancreatitis at Marseille, 1963. Bibl
Gastroenterol. 1965; 7: VII-VIII.
12. Singer MB, Gyr K, Sarles H. Revised
classification of pancreatitis. Report of the
Second International Symposium on the
Classification of Pancreatitis in Marseille,
France. March 28-30, 1984. Gastroenterology.
1985; 89(3): 683-685.
13. Sarner M, Cotton PB. Definition of acute and
chronic pancreatitis. Clin Gastroenterol. 1984;
13(3): 865-870.
14. Sarner M. Pancreatitis: definitions and
classification. In: Go VLW, Gardner JD,
Brooks FP, Lebenthal E, Di Magno EP,
Scheele GA, editors. The exocrine pancreas:
biology, pathobiology and diseases. New
York: Raven Press; 1986. p. 459-464.
15. Bittner R, Block S, Bchler M, Beger HG.
Pancreatic abscess and infected pancreatic
necrosis. Different local septic complications
in acute pancreatitis. Dig Dis Sci. 1987;
32(10): 1082-1087.
16. Beger HG. Surgery in acute pancreatitis.
Hepatogastroenterology. 1991; 38(2): 92-96.
17. Gazzaniga GM. Whats new on pancreatic
diseases: contribution to the updating course
on Pancreatic Diseases, Geneva, April 22-25,
1992; Stuttgart, New York: Georg Thieme
Verlag; 1994. p. 459-464.
18. Bradley EL. A clinically based classification
system for acute pancreatitis. Summary of the
International
Symposium
on
Acute
Pancreatitis, Atlanta, Ga, September 11-13,
1992. Arch Surg. 1993; 128(5): 586-590.
19. Bradley EL. A clinical based classification
system for acute pancreatitis. Ann Chir. 1993;
47(6): 537-541.

20. Bradley EL. The necessity for a clinical


classification of acute pancreatitis. The Atlanta
System. In: Bradley EL, editor, Acute
pancreatitis: Diagnosis and therapy. New
York: Raven Press Ltd; 1994. p. 27-32.
21. Banks PA. Practice guidelines in acute
pancreatitis. Am J Gastroenterol. 1997; 92(3):
377-386.
22. British Society of Gastroenterology. United
Kingdom guidelines for the management of
acute pancreatitis. Gut. 1998; 42(Suppl. 2):
S1-S13.
23. Bollen TL, Besselink MG, van Santvoort HC,
Gooszen HG, van Leeuwen MS. Toward an
update of the Atlanta classification on acute
pancreatitis: review of new and abandoned
terms. Pancreas. 2007; 35(2): 107-113.
24. Papachristou GI, Whitcomb DC. Predictors of
severity and necrosis in acute pancreatitis.
Gastroenterol Clin North Am. 2004; 33(4):
871-890.
25. Beger HG, Rau B, Isenmann R. Natural
history
of
necrotizing
pancreatitis.
Pancreatology. 2003; 3(2): 93-101.
26. Bhatia M, Wong FL, Cao Y, Lau HY, Huang
J, Puneet P, Chevali L. Pathophysiology of
acute pancreatitis. Pancreatology. 2005; 5(23): 132-144.
27. Lakisch PG, Pflichthofer D, Lehnick D. No
strict correlation between necrosis and organ
dysfunction determines outcome in acute
pancreatitis. Br J Surg. 2002; 89: 298-302.
28. Vege SS, Chari ST. Organ failure as an
indicator of severity of acute pancreatitis: time
to revisit the Atlanta classification.
Gastroenterology. 2005; 128(4): 1133-1135.
29. Johnson CD, Abu-Hilal M. Persistent organ
failure during the first week as a marker of
fatal outcome in acute pancreatitis. Gut. 2004;
53(9): 1340-1344.
30. Balthazar EJ, Robinson DL, Megibow AJ,
Ranson JH. Acute pancreatitis: Value of CT in
establishing prognosis. Radiology. 1990;
174(2): 331-336.
31. Balthazar EJ. Complications of acute
pancreatitis: clinical and CT evaluation.
Radiol Clin North Am. 2002; 40(6): 12111227.
32. Robinson PJ, Sheridan MB. Pancreatitis:
computed
tomography
and
magnetic
resonance imaging. Eur Radiol. 2000; 10(3):
401-408.
33. Chatzicostas C, Roussomoustakaki M, Vardas
E, Romanos J, Kouroumalis EA. Balthazar
computed tomography severity index is
superior to Ranson criteria and Apache II and
III scoring systems in predicting acute
pancreatitis outcome. J Clin Gastroenterol.
2003; 36(3): 253-260.

Pancreatita acut clasificarea Atlanta revizuit

125
Jurnalul de Chirurgie (Iai), 2013, Vol. 9, Nr. 2

34. Balthazar EJ, Freeny PC, van Sonnenberg E.


Imaging and intervention in acute pancreatitis.
Radiology. 1994; 193(2): 297-306.
35. Baron TH, Morgan DE, Vickers SM, Lazenby
AJ. Organized pancreatic necrosis endoscopic,
radiologic, and pathologic features of a distinct
clinical entity. Pancreas. 1999; 19(1): 105
108.
36. Banks PA, Freeman ML. Practice Parameters
Committee of the American College of
Gastroenterology (2006). Practice guidelines
in acute pancreatitis. Am J Gastroenterol.
2006; 101(10): 2379-2400.
37. Punescu V, Bordnc I, Popa C, Pop-Began
V, Pop-Began D. Ce operm? Cnd operm?
Cum operm pancreatita acut? Jurnalul de
Chirurgie (Iai). 2006; 2(4): 378391.
38. Pandol SJ, Saluja AK, Imrie CW, Banks PA.
Acute pancreatitis: bench to the bedside.
Gastroenetrology. 2007; 132(3): 1127-1151.
39. Bradley EL. A natural history based clinical
classification system for acute pancreatitis. In:
Bchler MW, Uhl W, Friess H, Malpertherner
P, editors. Acute pancreatitis novel concepts
in biology and therapy. Berlin, Viena:
Blackwell Science; 1999. p. 181-192.
40. Vege SS, Gardner TB, Chari ST, et al. Low
mortality and high morbidity in severe acute
pancreatitis without organ failure: A case for
revising the Atlanta classification to include:
Moderately severe acute pancreatitis. Am J
Gastroenterol. 2009; 104(3): 710-715.
41. Mofidi R, Patil PV, Suttie SA, Parks RW. Risk
assessment in acute pancreatitis. Br J Surg.
2009; 96: 137-150.
42. Tenner S, Sica G, Hughes M, et al.
Relationship of necrosis to organ failure in
severe acute pancreatitis. Gastroenterology.
1997; 113(3): 899-903.
43. Tenner S. Initial management of acute
pancreatitis: critical issues during the first 72
hours. Am J Gastroenterol. 2004; 99(12):
2489-2494.
44. Halonen K. Outcome prediction and quality of
live in severe acute pancreatitis. Academic
Disertation. Medical Faculty of the University
of Helsinky; Helsinky: 2004. p. 40-64.
45. Punescu V, Spircu T, Bordnc I, Popa C,
Crciunoiu M. Valoarea predictiv a
insuficienei multiple de organe n pancreatita
acut.
Chirurgia
(Bucureti).
2012;
107(Suppl.1): S323-S324.
46. Uomo G. Do we really need a new category of
severity for patients with acute pancreatitis?
Journal of Pancreas. 2009; 10(5): 583-584.
47. Isenmann R, Rau B, Beger HG. Early severe
acute pancreatitis: characteristics of a new
subgroup. Pancreas. 2001; 22(3): 274-278.

48. Sharma M, Banerjee D, Garg PK.


Characterization of newer subgroups of
fulminant and subfulminant pancreatitis
associated with a high early mortality. Am J
Gastroenterol. 2007; 102(12): 2688-2695.
49. Talkudar R, Vege SS. Classification of the
severity of acute pancreatitis. Am J
Gastroenterol. 2011; 106: 1169-1170.
50. Tran DD, Cuesta MA. Evaluation of severity
in patients with acute pancreatitis. Am J
Gastroenterol. 1992; 87(5): 604-608.
51. Petrov MS, Windsor JA. Classification of the
severity of acute pancreatitis: how many
categories make sense? Am J Gastroenterol.
2010; 105(1): 74-76.
52. Frey CF. Classification of pancreatitis: state of
the art. Pancreas. 1986; 1(1): 62-68.
53. Punescu V. Aspecte clinice i terapeutice n
pancreatita acut sever la nceputul secolului
In: Bdescu Th, Chira C, Lengyel DM, Radu
CM, editors, Tehnici moderne de investigaie
i perspective terapeutice n bolile digestive.
Bucuret: Editura Medical; 2011. p. 325-384.
54. French Consensus Conference on Acute
Pancreatitis:
Conclusions
and
Recommendations. Paris, France, January 2526, 2001. Eur J Gastroenterol Hepatol. 2001;
13(Suppl.4): S1-S13.
55. Yadav D, Agarwal N, Pitchumoni CS. A
critical evolution of laboratory tests in acute
pancreatitis. Am J Gastroenterol. 2002; 97(6):
1309-1318.
56. Isenmann Q. Classification of severe acute
pancreatitis. In: Beger HG, Matsuno S,
Cameron JL, editors, Diseases of the pancreas.
Current surgical therapy. Berlin, Heidelberg:
Springer-Verlag; 2008. p. 173-179.
57. Bollen TL, van Santvoort HC, Besselink MG,
et al. The Atlanta classification of acute
pancreatitis revisited. Br J Surg. 2008; 95(1):
6-21.
58. Acute Pancreatitis Classification Working
Group. Revision of the Atlanta classification
acute pancreatitis. 2008. [available online at
www.pancreasclub.com/wpcontent/uploads/2011/11/AtlantaClassification.
pdf]
59. Banks PA, Bollen TL, Dervenis C, et al. Acute
Pancreatitis
Classification
Group

Classification of acute pancreatitis - 2012:


revision of the Atlanta classification and
definitions by international consensus. Gut.
2013; 62(1): 102-111.
60. Vincent JL, Moreno R, Takala J, et al. The
SOFA
(Sepsis-related
Organ
Failure
Assessment) score to describe organ
dysfunction / failure. Intensive Care Med.
1996; 22(7): 707-710.

126

Punescu V.

Jurnalul de Chirurgie (Iai), 2013, Vol. 9, Nr. 2

61. Johnson CD. U.K. guidelines for the


management of acute pancreatitis. Gut. 2005;
54(Suppl.3): iii1 iii9.
62. Chauhan S, Forsmark CE. The difficulty in
predicting outcome in acute pancreatitis. Am J
Gastroenterol. 2010; 105(2): 443-445.

63. Miles KA, Griffiths MR. Perfusion CT: a


worthwhile enhancement? Br J Radiol. 2003;
76(904): 220-231.
64. Thoeni RF. The revised Atlanta classification
of acute pancreatitis: its importance for the
radiologist and its effect on treatment.
Radiology.
2012;
262(3):
751-764.

ARTICOLE DE SINTEZ

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CHIMIOTERAPIA HIPERTERMIC INTRAPERITONEAL


(CHIP) ASOCIAT CITOREDUCIEI TUMORALE N
TRATAMENTUL CARCINOMATOZEI PERITONEALE DE
ETIOLOGIE COLORECTAL
I. Huanu1,2, I. Radu1,2, B. Filip1,2, Mihaela Buna2, Maria Gabriela Aniei1,2,
M. Deraco3, V. Scripcariu1,2
1) Universitatea de Medicin i Farmacie Gr.T. Popa Iai
2) Clinica I Chirurgie Oncologic, Institutul Regional de Oncologie Iai
3) Department of Surgery, Fondazione IRCCS, Istituto Nazionale Tumouri Milano, Milano, Italia;
Peritoneal Surface Malignancy Program
HYPERTHERMIC INTRAPERITONEAL CHEMOTHERAPY WITH CYTOREDUCTIVE
SURGERY FOR THE TREATMENT OF PERITONEAL CARCINOMATOSIS FROM
COLORECTAL ORGIN (Abstract): Peritoneal carcinomatosis due to gastrointestinal
malignancies has been considered a poor prognosis entity. Few prospective studies have shown 6
to 12 months suvirval period for peritoneal carcinomatosis of colorectal cancer (CR) treated with
systemic chemotherapy. New chemotherapeutic agents and monoclonal antibodies increased
survival to 16-22 months. Despite this new systemic treatment most patients will die due to
cachexia, peritonitis and/or intestinal occlusion. Normothermic or hyperthermic intraperitoneal
chemotherapy, intraoperative or early postoperative became in the last three decades the standard
treatment for several malignancies of peritoneum and it has proven effective in peritoneal
carcinomatosis of colorectal and ovarian origin. The main drawbacks of this method is lack of
studies to confirm the benefits. A long learning curve, high morbidity and mortality, lack of
studies on quality of life and the high cost of this procedure appears to be the most important
disadvantages of this method. Recent studies including carreful selected patients show a five year
suvirval rate of 40%, median survirval period of 30 months, high morbidity (up to 60%) and a
mortality up to 8%. Phase III trials on patients with peritoneal carcinomatosis from colorectal
cancer treated with HlPEC are still ongoing. We present and review the latest results from the
literature regarding the value of HIPEC in peritoneal carcinomatosis from colorectal origin.
KEY WORDS: PERITONEAL CARCINOMATOSIS; COLORECTAL CANCER; HYPERTHERMIC INTRAPERITONEAL CHEMOTHERAPY; HIPEC; CYTOREDUCTIVE
SURGERY
SHORT TITLE: Chimioterapia hipertermic intraperitoneal (CHIP) n CCR
Hyperthermic intraperitoneal chemotherapy (HIPEC) in CRC
HOW TO CITE: Huanu I, Radu I, Filip B, Buna M, Deraco M, Scripcariu V. [Hyperthermic intraperitoneal
chemotherapy with cytoreductive surgery for the treatment of peritoneal carcinomatosis from colorectal orgin] Jurnalul de
chirurgie (Iai). 2013; 9(2): 127-136. DOI: 10.7438/1584-9341-9-2-3.

INTRODUCERE
Cancerul colorectal (CCR) are n
Europa o inciden anual de 415.000 cazuri
[1]. Mortalitatea anual este estimat la peste
200.000 decese [1].
Carcinomatoza peritoneal (CP) este
una din cile de diseminare ale cancerului

CCR. Acest tip de evoluie a CCR poate


apare izolat fr metastaze sau adenopatii,
uneori fiind rezultatul rupturii tumorii n
peritoneu (spontan sau n timpul actului
chirurgical). Nu are o simptomatologie
particular, tabloul clinic suprapunndu-se
pe cel al tumorii primitive. Cu toat

Received date: 28.01.2013


Accepted date: 01.03.2013
Adresa de coresponden: Prof. Dr. Viorel Scripcariu
Clinica I Chirurgie Oncologic, Institutul Regional de Oncologie Iai
Str. General Henry Mathias Berthlot nr. 2-4, 700483, Iai
Tel.: 0040 (0) 374 27 88 10
Fax: 0040 (0) 374 27 88 02
E-mail: vscripcariu@gmail.com

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dezvoltarea tehnicilor de imagerie, datorit


sensibilitii i specifictii reduse a
examenelor imagistice volum-dependente n
evidenierea modificrilor de la nivelul
seroasei peritoneale, CP este frecvent o
descoperire intraoperatorie (Fig. 1). Aceleai
dificulti sunt prezente i n supravegherea
postoperatorie a pacienilor operai pentru
CCR.

Fig. 1 Carcinomatoz peritoneal metacron la un


pacient operat pentru cancer de colon drept
(colecia Prof. Dr. Viorel Scripcariu)

EPIDEMIOLOGIE
Incidena
CP
este
estimat
la aproximativ 4-10% din pacienii cu CCR
[2-4].
ntr-un studiu retrospectiv [2] publicat
n 2002 pe un lot de 3019 pacieni operai
pentru CCR Jayne i colab. a identificat 349
pacieni (13%) care au prezentat CP. Din cei
349 de pacieni, 214 au prezentat CP
sincron iar 135 au prezentat CP metacron
tumorii primitive. Din cei 214 pacieni cu
CP sincron 125 (58%) nu prezentau alt
localizare detectabil prin explorrile
imagistice deci localizarea peritoneal era
unic iar din acetia 80 prezentau CP
limitat.
ntr-un studiu populaional pe o
perioad cuprins ntre 1995 i 2008,
Lemmens i colab. [3] au observat la un
numr de 18.300 de pacieni diagnosticai cu
CCR 904 pacieni cu CP sincron
reprezentnd 4,8% din totalul cazurilor i
24% din pacienii cu boal metastatic. Din
pacienii cu CP, 40% aveau peritoneul ca
unic localizare. Analiza multivariat a

relevat ca factori de risc pentru descoperirea


CP sincrone stadiul T4 (risc de 4 ori mai
mare dect T2), statusul ganglionar (risc
sczut de 10 ori la pacienii cu N0 fa de cei
N+), gradul de difereniere, vrsta sub 60 de
ani, varianta mucinoas i localizarea pe
colonul drept).
Recent, Segelman i colab. [4] au
publicat rezultatele unui studiu referitor la
incidena CP la pacienii diagnosticai cu
CCR n regiunea Stockholm n perioada
1995-2007. Existena unui Registru Naional
i a unui Registru Regional n care sunt
inclui pacienii cu CCR cu probabilitate
minim de pierdere din eviden a facilitat
efectuarea acestui studiu. n cei 12 ani au
fost diagnosticai, la o populaie regional de
aproximativ 2,1 milioane locuitori 11.200
pacieni cu CCR. Dintre acetia, 924 pacieni
reprezentnd 8,3% au prezentat CP sincron
sau metacron: 4,3% din pacieni aveau CP
sincron iar 4,5% au dezvoltat CP dup
interveniile chirurgicale.
TRATAMENTUL CLASIC AL
CP DE ORIGINE COLORECTAL
(chimioterapie sistemic i tratament
chirurgical conservator)
Puinele studii prospective efectuate au
artat o supravieuire medie n jur de 6 luni
la pacienii cu chimioterapie sistemic
clasic i tratament chirurgical paliativ, de
citoreducie sau/i bypass. Este dificil de
apreciat impactul chimioterapiei sistemice
izolat sau asociat cu o intervenie
chirurgical n CP de etiologie CCR, ntruct
CP a fost mult timp considerat boal
sistemic, incurabil, iar tratamentul a fost
raportat n studii mpreun cu alte localizri
metastatice sau boal avansat local i
nerezecabil.
ntr-un studiu retrospectiv Pelz i
colab. [5] au comparat supravieuirea
pacienilor n funcie de chimioterapia
primit. Au fost urmrii 1.920 pacieni cu
CCR operai pe o perioad cuprins ntre
1997-2006. Dintre acetia, 240 (13%) au
prezentat CP din care 98 (42%) sincron i
142 (58%) metacron. 38% din pacienii cu
CP aveau localizare unic limitat la
peritoneu. Pacienii cu CP au fost mprii

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n 3 loturi: fr chimioterapie, chimioterapie


cu 5-Fluorouracil i Leucovorin i un lot ce
includea i Oxaliplatin sau irinotecan asociat
sau nu cu ageni biologici. Supravieuirea
medie a fost de 5 luni la cei far
chimioterapie, 11 luni la cei cu 5Fluorouracil i Leucovorin i 12 luni la cei la
care s-a asociat Oxaliplatin sau Irinotecan,
iar global, pe ntreg lotul, la 3 i 5 ani a fost
de 6 i respectiv, 3%. Din punct de vedere
statistic supravieuirea a fost influenat de
efectuarea chimioterapiei, dar regimul
utilizat nu a influenat n final supravieuirea.
Acest rezultat este oarecum n contradicie
cu concluziile altor studii cu supravieuire de
pn la 22 de luni n chimioterapia sistemic
complex ce include oxaliplatin sau
irinotecan.
Chirurgia conservatoare de by-pass,
enterostomie, colostomie are un efect
imprevizibil asupra supravieuirii pacienilor
[6]. Acetia decedeaz la cteva sptmni
postoperator. La complicaiile bolii se
adaug i posibilele complicaii ale actului
chirurgical. Tratamentul fistulelor i
complicaiilor de tip peritonitic este dificil i
grevat de un prognostic sumbru.
TRATAMENTUL
CP
PRIN
CHIMIOTERAPIE
SISTEMIC
I
AGENI BIOLOGICI
Odat cu progresele din bioinginerie
care au permis sinteza la scar industrial,
terapia cu ageni biologici din clasa
anticorpilor monoclonali a devenit din ce n
ce mai folosit n tratamentul cancerelor
avansate sau metastatice. n urma studiilor
de biologie molecular s-au evideniat mai
multe poteniale inte de atac n tratamentul
tumorilor solide: inhibitori de factori de
cretere
derivat
din
endoteliu
(Bevacizumab), inhibitori ai receptorului
factorului de cretere derivat din epiderm
(Cetuximab, Panitumumab), inhibitori ai
receptorului
extracelular
al
unei
glicoproteine implicate n transportul
transmembranar de Ca2+(Catumaxomab).
n urma rezultatelor bune ale
chimioterapicelor de clas nou n
tratamentul CCR cu metastaze nerezecabile

la nivel hepatic s-a ncercat utilizarea


acestora i n tratamentul CP. Sunt puine
studii referitoare la adiia agenilor biologici
n tratamentul CP de origine CCR i loturile
de pacieni incluse n studii n general nu
depesc 50 de pacieni.
ntr-un studiu retrospectiv pe un lot de
50 de pacieni [7] supravieuirea medie a fost
de 12 luni n lotul de pacieni tratai cu 5
Fluorouracil i Oxaliplatin i 17 luni la
pacienii care au primit n plus i ageni
biologici. La pacienii la care agenii
biologici au fost introdui ca prim linie
terapeutic supravieuirea a fost de 22 luni.
Un alt studiu [8] a evaluat retrospectiv
50 de pacieni cu CP CCR tratai cu diverse
scheme de chimioterapie sistemic. La 22 de
pacieni n tratament au fost inclui i ageni
biologici. Pacienii cu ageni biologici au
avut o supravieuire medie de 18 luni,
semnificativ mai bun dect a pacienilor
tratai fr ageni biologici. La pacienii la
care agenii biologici au fost introdui n
prima linie de tratament, supravieuirea
medie a fost de aproximativ 23 de luni.
TRATAMENTUL
CP
PRIN
CHIRURGIE DE CITOREDUCIE I
CHIMIOTERAPIE NORMO- I HIPERTERMIC INTRAPERITONEAL
Administrarea
intraperitoneal
a
citostaticelor concomitent (Fig. 2) cu
citoreducia tumoral optimal (Fig. 3), care
are drept obiectiv disecia tuturor aderenelor
de la vechile intervenii i ablaia maselor
tumorale n aa fel nct rezidiul tumoral s
fie mai mic de 2-3 mm grosime, a fost
propus pentru a crete concentraia local a
chimioterapeuticului limitnd toxicitatea
sistemic pentru c studiile in vitro au artat
c citostaticele administrate n circulaia
sistemic
depesc
greu
bariera
peritoneoplasmatic [9].
n 1995 Sugarbaker i colab. [10] au
publicat primele rezultate ale chimioterapiei
normotermice intraperitoneale pe un lot de
181 pacieni operai pentru CP de origine
CCR (51 pacieni) i apendicular (130
pacieni). Autorii au identificat ca factori
prognostici negativi originea colonic,

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statusul ganglionar, diferenierea tumoral i


extensia CP. Pentru pacienii cu origine
CCR, cu citoreducie incomplet autorii au
raportat o supravieuire la 3 ani de 20%,
semnificativ mai mic dect supravieuirea
celor la care s-a practicat o citoreducie
complet (60%).

Fig. 2 Chimioterapie hipertermic n sistem abdomen


nchis (colecia Dr. Marcello Deraco)

Fig. 3 Peritonectomie pelvin la un pacient cu


carcinomatoz peritoneal cu punct de plecare tumor
de jonciune rectosigmoidian
(colecia Dr. Marcello Deraco)

Exist un singur studiu [11]


randomizat, finalizat pn n prezent,
referitor la CP cu origine CCR, tratai prin
chimioterapie hipertermic intraperitoneal
(CHIP) care include 105 pacieni operai n
perioada februarie 1998 - august 2001.
Criteriile de includere au fost: diagnostic
histologic de CP de origine CCR, absena
metastazelor hepatice sau extra-abdominale,
vrsta sub 71 de ani, status de performan
acceptabil, cu funcia renal, hepatic i
medular n limite normale.

Pacienii au fost mprii n dou


loturi, randomizate, pentru tratamentul
standard i respectiv pentru tratamentul
experimental (CHIP). Pacienii din grupul
standard (51 de pacieni dup randomizare)
au fost operai doar n caz de apariie a unor
complicaii (n aceast situaie s-a practicat o
intervenie paliativ - by-pass, stentare i rar
rezecie), iar 44 au primit chimioterapie
sistemic dup standardul acelei perioade
din Olanda - 5-Fluorouracil i Leucovorin.
Cei 54 de pacieni din grupul CHIP, au fost
operai practicndu-se citoreducie tumoral
la 49 de pacieni asociat CHIP pe o
perioad de 90 de minute cu Mitomicin-C.
Ulterior, o parte din aceti pacieni (33
pacieni) au efectuat chimioterapie sistemic
dup aceeai schem (5-Fluorouracil i
Leucovorin). Toi pacienii au fost ulterior
reevaluai la fiecare 3-6 luni. Rezultatele
studiului au artat o supravieuire median
de 12 luni n braul cu chimioterapia
sistemic i tratament chirurgical paleativ i
de 22 de luni n braul CHIP deci un
beneficiu de aproximativ 10 luni.
Au fost aduse unele reprouri aduse
acestui studiu. Unul dintre ele se refer la o
rat nalt a morbiditii i mortalitii
postoperatorii: morbiditatea de gradul IV de
45% (cu 15% fistule intestinale, pancreatit
2%, insuficien renal 6%) i respectiv,
mortalitate de 8%. Studiile ulterioare au
artat o scdere a morbiditii i mortalitii
prin ajustarea dozelor de chimioterapic
intraperitoneal i ameliorarea tehnicii
chirurgicale odat cu parcurgerea curbei de
nvare [12]. Un alt repro a fost includerea
n studiu a pacienilor cu cancere
apendiculare care au un prognostic mai bun,
dar acetia au fost n numr sensibil mai
mare n braul clasic al studiului influennd
astfel mai puin supravieuirea n braul
experimental. Markman [13] reproeaz
designul studiului: autorii ar fi trebuit s
evalueze comparativ ntre citoreducie
tumoral optimal i chimioterapie sistemic
ntr-un lot i n cellalt lot citoreducie
tumoral
optimal
i
chimioterapie
intraperitoneal i apoi chimioterapie
sistemic.

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n 2010 Glehen i colab. [14] au


prezentat rezultatele unui studiu multicentric
ce includea 22 de spitale din Frana n care
din 1290 de pacieni tratai prin CHIP, 523
erau cu CP de origine CCR. Pe lng pacieii
cu CP de origine CCR au fost inclui n
studiu i 301 pacieni cu pseudomixoma
peritonei, autorii specificnd astfel clar
etiologia diferit a CP a dou entiti cu
prognostic diferit. Restul pacienilor
prezentau CP de etiologie gastric - 159 de
pacieni, adenocarcinom apendicular - 50 de
pacieni i 88 cu mezoteliom peritoneal
difuz. Pe ntreg lotul, 90% dintre pacieni
aveau statusul de performan (O.M.S.) de 0
sau 1. La 34% dintre cazuri CP a fost o
descoperire intraoperator. 19% din pacieni
au fost examniai pentru dureri abdominale.
La 10% a fost decelat n urma unor
examene imagistice de rutin. La mai puin
de 10% din pacieni, diagnosticul a fost pus
cu ocazia unor complicaii (3,7% ocluzii
intestinale, apendicite sau peritonite 1%,
hernii simptomatice 1,5%). Alte motive de
prezentare ale pacienilor cu CP au fost
creterea circumferinei abdominale la 10%,
fatigabilitate i scdere ponderal la 5%,
creterea valorii markerilor tumorali la 2%
din pacieni. Pentru pacienii operai cu CP
de origine CCR, mediana supravieuirii a
fost de 30 de luni, iar supravieuirile la 3 i 5
ani au fost de 41 i respectiv 26%. Analiza
univariat efectuat a relevat ca factori de
prognostic negativi vrsta pacienilor peste
61 de ani, prezena metastazelor hepatice,
sexul masculin, statusul de performan
precar, experiena centrului n care a
fost efectuat procedura, interesarea
limfonodulilor, chimioterapia preoperatorie,
tipul de chimioterapie perioperatorie
efectuat, utilizarea oxaliplatinului, durata
perfuziei i calitatea citpreduciei.
Elias i colab. [15] au prezentat n
2011 rezultatele unui studiu referitor la
incidena i tratamentul CP dup chirurgia
electiv la persoanele apreciate cu risc
pentru dezvoltarea CP. Pe un lot de 41 de
pacieni operai pentru CCR pe care autorii iau considerat de risc pentru dezvoltarea CP
(CP limitat complet rezecat, tumori

Krukenberg rezecate odat cu tumora de


colon i tumori perforate n timpul diseciei)
i la care examenul CT i markerii tumorali
erau n limite normale neridicnd
suspiciunea de boal recidivat, practic
relaparotomie la aproximativ 1 an. La 23 de
pacieni autorii au evideniat CP. Toi cei 41
de pacieni au fost tratai prin CHIP asociat
la cei 23 cu CP evident i cu peritonectomie
i citoreducie. Supravieuirea i absena
semnelor de boal la 5 ani a fost de 90% i
respectiv 43%. Un singur pacient a decedat
postoperator la 69 zile dup intervenie.
Concluzia autorilor a fost c o intervenie
second-look la pacienii cu risc s dezvolte
CP ar aduce beneficii oncologice limitnd
morbiditatea postoperatorie.
n prezent sunt n desfurare mai
multe studii de faz II i III referitoare la CP
de origine CCR.
ProphyloCHIP
(ClinicalTrials.gov
Identifier NCT-01226394) este un trial
randomizat multicentric francez n curs de
recrutare de pacieni dup intervenii cu viz
curativ pe tumori CR cu risc de dezvoltare
de CP. Autorii studiului ProphyloCHIP au
propus ca dup intervenia chirurgical i
chimioterapia sistemic efectuat cu 5Fluorouracil, Leucovorin i Oxaliplatin timp
de 6 luni pacienii s fie reevaluai la 6-8
luni de la terminarea chimioterapiei.
Pacienii fr semne de recidiv peritoneal
la examenul CT i fr creteri ale valorilor
markerilor vor fi randomizai n dou loturi.
Lotul standard este format din pacieni care
vor fi urmrii i vor fi operai doar n cazul
apariiei semnelor de CP sau metastaze n alt
teritoriu. Lotul experimental este format din
pacieni la care se practic o laparotomie
exploratorie i dac este prezent CP se
practic citoreducie tumoral i CHIP iar
dac nu exist CP se practic doar CHIP.
Studiul urmrete s evalueze difereele de
supravieuire la 3 i 5 ani ntre cele dou
loturi de pacieni.
n 2010, National Institute for Health
and Clinical Excellence din Marea Britanie
(http://www.nice.org.uk/guidance/IPG331/
PublicInfo) a recomandat ca chimioterapia
hipertermic intraperitoneal s poat fi

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considerat o alternativ la tratamentul


sistemic la pacienii cu CP de origine CCR i
a ncurajat efectuarea de studii clinice n
acest sens. De asemenea, ghidurile
terapeutice franceze [16] ncepnd din 2010
recomand procedura complex ca terapie
individualizat la pacienii atent selecionai
cu CP de origine CCR.
CP DESCOPERIT INCIDENTAL
Nu exist un consens asupra terapiei
optime a CP de origine CCR la pacienii la
care explorrile iniiale nu indicau prezena
acesteia. Atunci cnd este descoperit n
timpul
interveniilor
pentru
CCR
recomandrile [17] depind de aspectul
intraoperator. Pentru tumorile neobstructive,
cu carcinomatoz limitat cea mai bun
opiune terapeutic ar fi limitarea
interveniei la biopsiere, nregistrarea
localizrii CP i trimiterea pacientului pentru
evaluarea de ctre o echip multidisciplinar
cu experien n CHIP. Pentru pacienii la
care intervenia este fcut n urgen
(perforaie, hemoragie, ocluzie) indicaia
este de rezecie colonic sau colostomie n
amonte i limitare a diseciei peritoneale
pentru a facilita o intervenie cu intenie
curativ ulterioar.
CITOREDUCIE
TUMORAL
FR CHIP
Nu se cunosc efectele chimioterapiei
sistemice la pacienii cu CP cu origine CCR
la care s-a practicat o citoreducie tumoral
optimal. ntr-un articol publicat n 2012
Matsuda i colab. [18] au evaluat
retrospectiv 149 pacieni cu CP cu origine
CCR operai n perioada 1997-2008. Dintre
aceti pacieni, 31 au fost diagnosticai cu
CP sincron i la ei s-a practicat citoreducie
tumoral complet i peritonectomii pariale
pn la absena vizualizrii de depozite
tumorale
intraperitoneale,
ulterior
administrndu-se chimioterapie sistemic.
La niciun pacient nu s-a practicat
chimioterapie intraperitoneal. Din aceti 31
de pacieni 24 au prezentat recidiv
tumoral.

Supravieuirea la 5 ani a fost de 36% la


pacienii cu citoreducie complet. 77% din
pacienii operai au dezvoltat boal
extraperitoneal.
SELECIA
PACIENILOR
PENTRU CHIP
Selecia pacienilor cu CP de origine
CCR pentru CHIP nu este uoar. Decizia de
tratament chirurgical nu ar trebui s aparin
unui singur medic, ea ar trebui s fie luat n
consens de ctre echipa multidisciplinar
care urmrete pacientul [19].
Nu exist un algoritm care s selecteze
secvena terapeutic adecvat i care s
permit selecia pacientului i nici studii
despre chimioterapia cu intenie de
neoadjuvan. Decizia trebuie s in cont de
riscuri i de rezultatele obinute imediat i
mcar pe termen mediu i este strns legat
de curba de nvare [12].
Piso i colab. [20] au stabilit criterii
orientative de selecie i de respingere
pacienilor cu CP propui pentru intervenie
chirurgical identificnd factori legai de
tumor i factori legai de pacient:
1) Factori legai de tumor: localizarea
tumorii primitive (prognostic mai prost
pentru cele rectale), tip i grading
histologic, afectarea extra-abdominal,
boala
metastatic,
prezena
metastazelor limfoganglionare paraaortice, Peritoneal Cancer Index [21]
(n baza mai multor studii retrospective recomandarea este s fie
propui pentru intervenia chirurgical
acei pacieni cu un indice mai mic de
10-12), interesarea intestinului subire,
interesarea ligamentului hepatogastric,
stenoza biliar sau ureteral, rspunsul
la chimioterapia sistemic anterioar.
2) Factori legai de pacient: statusul de
performan, comorbiditile, calitatea
vieii presupus postoperator.
3) Factori ce in de personalul medical:
curba de nvare i experiena echipei
chirurgicale.

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CHIRURGIE DE CITOREDUCIE
ASOCIAT CHIP: MORBIDITATE I
MORTALITATE
CHIP este o intervenie complex, cu
durat ce poate depi 10 ore, cu necesitatea
uneori de rezecii multiviscerale, cu risc de
tulburri de coagulare ce pot necesita
administrarea snge i plasm n cantiti
mari, la care se adaug consecinele
chimioterapiei intraperitoneale i ale
hipertermiei. CHIP are deci o rat ridicat de
morbiditate i mortalitate postoperatorieceea
ce ridic semne de ntrebare asupra
raportului risc / beneficii pentru pacieni cu
CP [22].
n centrele cu experien mortalitatea
este de 2-3% iar morbiditatea de 25-40%
[23-25]. Cele mai frecvente complicaii
chirurgicale
includ:
dehiscenele
anastomotice, perforaiile intestinale, ileusul
prelungit, pancreatita, sepsisul intraabdominal,
hemoragia
postoperatorie,
embolia pulmonar, insuficiena renal,
toxicitatea hematologic.
Creterea numrului de intervenii
efectuate amelioreaz rata de morbiditate i
mortalitate fiind raportate serii cu mortalitate
zero i mobiditate de 20-30% n centrele cu
peste 100 de cazuri operate [26]. Dup
Verwaal rata de complicaii este mai mare cu
ct extensia CP este mai mare deoarece
aceasta presupune o intervenie mai de
anvergur [11].
CALITATEA VIEII DUP CHIP
Una dintre principalele obiecii la
tratamentul complex al CP este cea
referitoare la calitatea vieii pacienilor n
perioada postoperatorie. Este ndoielnic c
un pacient vrstnic cu o colectomie total,
enterectomie ntins i gastrectomie total cu
absena tumorii reziduale dup o intervenie
chirurgical va avea o bun calitate a vieii.
Pe de alt parte un pacient de 40 de ani cu o
peritonectomie parietal i o colectomie
limitat pentru CP de origine CCR are toate
ansele ca la 12 luni postoperator s
desfoare activiti compatibile cu vrsta
sa. McQuellon i colab. [27] ntr-un studiu
efectuat pe un lot de 64 de pacieni operai

pentru CP de cauz digestiv, utiliznd


formularele de calitatea vieii FACT-C, a
notat c imediat postoperator calitatea vieii,
statusul emotional i cel fizic sunt n scdere
progresiv pn la 3 luni iar ulterior, se
remarc o mbuntire a calitii vieii pn
la 1 an (74% din pacieni sunt capabili la 12
luni postoperator s desfoare singuri peste
50% din activitatea cotidian fa de 19%
din pacieni la 3 luni).
COSTUL CHIP
Sunt puine studii referitoare la costul
interveniilor chirurgicale n contextul CHIP.
Este dificil de apreciat preul necesar pentru
prelungirea supravieuirii cu cteva luni sau
necesitatea modificrii schemelor de
tratament post CHIP. Metodologia de calcul
a costului interveniilor este una dificil, cu
luarea n calcul a tuturor costurilor pe durata
spitalizrii iar n unele cazuri costul pe
intervenie pare exagerat depind 130.000
euro.
ntr-un studiu publicat n 2003
Bonastre i colab. [28] estimeaz un cost
mediu de 38.000 euro per pacient operat i o
rambursare din partea statului francez de
20.000 euro per pacient rezultnd un deficit
de 18.000 euro la fiecare pacient. n 2008
aceeai autori public o analiz retrospectiv
pe un lot de 93 de pacieni operai prin
CHIP. Autorii estimeaz o prelungire a
supravieuirii la aceti pacieni cu
aproximativ 9 luni per pacient i estimeaz
costul prelungirii cu un an a vieii la 58.000
euro.
ntr-un articol din 2010 Killian i
colab. [29] pe un lot de 18 pacieni operai la
Spitalul Universitar Charite din Berlin
evalueaz costul mediu de spitalizare la
21.000 euro (o spitalizare medie n secia
reanimare de 6 zile).
CURBA DE NVARE N CHIP
I CHIRURGIA CITOREDUCTIV
Numeroase studii au artat c
prognosticul oncologic al pacienilor
depinde de experiena chirurgului [30].
Curba de nvare nu se refer numai la
efectuarea unei intervenii chirurgicale, n ea

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sunt incluse practic toate procedurile


efectuate de chirurg n selecia pacienilor,
selecia secvenei terapeutice, management
intra- i postoperator, anestezie, reanimare,
nursing postoperator, suport nutriional i
tratarea complicaiilor.
Smeenk i colab. [12] consider c
vrful curbei de nvare este atins dup
aproximativ 130 de cazuri. Autorii au
observat o reducere a morbiditii de la 71%
la 34%, o scdere a duratei de spitalizare de
la 24 la 17 zile i o cretere a procentului de
pacieni cu citoreducie complet de la 35 la
65% pe un lot de 323 pacieni operai pentru
CP de origine CCR sau apendicular
mprind pacienii n 3 loturi funcie de
perioada de timp n care au fost operai.
Mortalitatea postoperatorie a sczut de la 8%
la 4% dup primii 75 de pacieni operai.
Una din explicaiile autorilor pentru
rezultatele mai bune n timp este legat de o
selecie mai riguroas a pacienilor
excluznd pacieni cu CP extins la 6-7
regiuni abdominale - dificil de citoredus
complet i cu risc de complicaii
postoperatorii datorit exciziilor necesare
pentru o citoreducie optimal.
Una din consecinele practice ale
studiului curbei de nvare pentru
interveniile de mare amploare n afeciuni
chirurgicale relativ rare este necesitatea
centralizrii cazurilor [31]. Cazurile dificile,
cu potenial de morbiditate i mortalitate
ridicat ar trebui operate n centre specializate
de un numr limitat de chirurgi cu
experien n domeniu care au depit curba
de nvare i care au nceput primele cazuri
asistai de experi n domeniu. Rolul
turorelui este de a scurta aceast curb de
nvare. Pentru iniierea unui program nou
ntr-o instituie probabil c cea mai bun
strategie este instruirea participanilor din
acel program ntr-un centru de referin n
acel domeniu i apoi efectuarea primelor
intervenii ajutat de acel tutore.
CONCLUZII
Nu exist un tratament standard n CP
de origine CCR, diferitele metode de
tratament fiind discutate n funcie de

particularitile clinice, imagistice i


biologice ale pacientului.
Odat cu apariia unor noi clase de
chimioterapice prognosticul n CP de origine
CCR s-a mbuntit dar n ciuda rspunsului
iniial favorabil marea majoritate a
pacienilor prezint recidiv tumoral iar
supravieuirile la 5 ani sunt foarte rare.
Chimioterapia intraoperatorie normotermic, apoi n condiii de hipertermie a
devenit o alternativ la chimioterapia
sistemic cu intenie paleativ. Ideea de a
pune n contact direct celulele tumorale cu
agentul chimioterapic a trebuit s parcurg
mai multe etape pentru a fi acceptat.
n Romnia, dei exist preocupri
pentru tratamentul CP [32], nu sunt nfiinate
centre n care procedura complex s fie
folosit frecvent. Prin nfiinarea unor astfel
de centre, un numr limitat de pacieni cu CP
de etiologie CCR (estimat prin aproximaie
n baza studiului lui Jane i colab. [2] la
aproximativ 240 de cazuri/an), pseudomixoma peritonei i mezoteliom peritoneal
difuz ar putea beneficia de un tratament n
urma cruia prognosticul ar fi mbunti sau
ar putea fi chiar vindecai.

CONFLICTE DE INTERESE
Autorii nu declar niciun conflict de
interese.
RECUNOATERE
Acest studiu este rezultatul cercetrii
din cadrul unei burse doctorale din
proiectului U.M.F. Iai n parteneriat cu
UMF Timooara, Burse doctorale pentru
doctoranzi competitivi n Aria European a
Cercetrii POSDRU/1.5/88/S/ID proiect
63117.
O parte din activitatea de cercetare s-a
desfurat n Istituto Nazionale Tumouri,
Milano, Italia, n cadrul programului
Peritoneal Surface Malignancy Program,
sub coordonarea Dr. Marcello Deraco, Dr.
Dario Baratti i Dr. Shigeki Kusamura,
crora a dori s le mulumesc pentru
sprijinul acordat.

Chimioterapia hipertermic intraperitoneal (CHIP) n CCR

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BIBLIOGRAFIE
1. Bae JH, Lee JM, Ryu KS et al. Treatment of
ovarian cancer with paclitaxel- or carboplatinbased
intraperitoneal
hyperthermic
chemotherapy during secondary surgery.
Gynecol Oncol. 2007; 106: 193-200.
2. Jayne DG, Fook S, Loi C, Seow-Choen F.
Peritoneal carcinomatosis from colorectal
cancer. Br J Surg.2001; 89: 1545-1550.
3. Lemmens VE, Klaver YL, Verwaal VJ, Rutten
HJ, Coebergh JW, de Hingh IH. Predictors and
survival
of
synchronous
peritoneal
carcinomatosis of colorectal origin: a
population-based study. Int J Cancer. 2011;
128: 2717-2725.
4. Segelman J, Granath F, Holm T, Machado M,
Mahteme H, Martling A. Incidence,
prevalence and risk factors for peritoneal
carcinomatosis from colorectal cancer. Br J
Surg. 2012; 99: 699-705.
5. Pelz JO, Chua TC, Esquivel J et al. Evaluation
of best supportive care and systemic
chemotherapy as treatment stratified according
to the retrospective peritoneal surface disease
severity score (PSDSS) for peritoneal
carcinomatosis of colorectal origin. BMC
Cancer. 2010; 10: 689.
6. Averbach AM, Sugarbaker PH. Recurrent
intraabdominal
cancer
with
intestinal
obstruction. Int Surg. 1995; 80: 141-146.
7. Jacquet P, Stephens AD, Averbach AM et al.
Analysis of morbidity and mortality in 60
patients with peritoneal carcinomatosis treated
by cytoreductive surgery and heated
intraoperative intraperitoneal chemotherapy.
Cancer. 1996; 77: 2622-2629.
8. Klaver YL, Leenders BJ, Creemers GJ et al.
Addition of biological therapies to palliative
chemotherapy prolongs survival in patients
with peritoneal carcinomatosis of colorectal
origin. Am J Clin Oncol. 2013; 36(2): 157-161.
9. Sticca RP, Dach BW. Rationale for
hyperthermia
with
intraoperative
intraperitoneal chemotherapy agents. Surg
Oncol Clin N Am. 2003; 12: 689-701.
10. Sugarbaker PH, Jablonski KA. Prognostic
features of 51 colorectal and 130 appendiceal
cancer patients with peritoneal carcinomatosis
treated by cytoreductive surgery and
intraperitoneal chemotherapy. Ann Surg. 1995;
221: 124-132.
11. Verwaal VJ, van Ruth S, de Bree E et al.
Randomized trial of cytoreduction and
hyperthermic intraperitoneal chemotherapy
versus systemic chemotherapy and palliative
surgery
in
patients
with
peritoneal
carcinomatosis of colorectal cancer. J Clin
Oncol. 2003; 21: 3737-3743.

12. Smeenk RM, Verwaal VJ, Zoetmulder FA.


Learning curve of combined modality
treatment in peritoneal surface disease. Br J
Surg. 2007; 94: 1408-1414.
13. Markman M. Hyperthermic intraperitoneal
chemotherapy in the management of ovarian
cancer: A critical need for an evidence-based
evaluation. Gynecol Oncol. 2009; 113: 4-5.
14. Glehen O, Gilly FN, Boutitie F et al. Toward
curative treatment of peritoneal carcinomatosis
from nonovarian origin by cytoreductive
surgery
combined
with
perioperative
intraperitoneal chemotherapy: a multiinstitutional study of 1,290 patients. Cancer.
2010; 116: 5608-5618.
15. Elias D, Honore C, Dumont F et al. Results of
systematic second-look surgery plus HIPEC in
asymptomatic patients presenting a high risk
of
developing
colorectal
peritoneal
carcinomatosis. Ann Surg. 2011; 254: 289-293.
16. Taniguchi M, Ochiai M, Sakurai Y,
[Experimental study of intraperitoneal
hyperthermic chemotherapy]. Gan To Kagaku
Ryoho. 1998; 25: 1083-1086.
17. Liberale G, Van Den Eynde M, Hendlisz A, El
Nakadi I. Recommendations for general
surgeons
facing
incidental
peritoneal
carcinomatosis of colorectal origin. Eur J Surg
Oncol. 2008; 34: 725-726.
18. Matsuda K, Hotta T, Takifuji K et al. Clinical
impact of a macroscopically complete
resection of colorectal cancer with peritoneal
carcinomatosis. Surgery. 2010; 151: 238-244.
19. Esquivel J, Elias D, Baratti D, Kusamura S,
Deraco M. Consensus statement on the loco
regional treatment of colorectal cancer with
peritoneal dissemination. J Surg Oncol. 2008;
98: 263-267.
20. Piso P, Glockzin G, von Breitenbuch P et al.
Patient selection for a curative approach to
carcinomatosis. Cancer J. 2009; 15: 236-242.
21. Jacquet P, Vidal-Jove J, Zhu B, Sugarbaker P.
Peritoneal carcinomatosis from gastrointestinal
malignancy: natural history and new prospects
for management. Acta Chir Belg. 1994; 94:
191-197.
22. Chua TC, Yan TD, Saxena A, Morris DL.
Should
the
treatment
of
peritoneal
carcinomatosis by cytoreductive surgery and
hyperthermic intraperitoneal chemotherapy
still be regarded as a highly morbid
procedure?: a systematic review of morbidity
and mortality. Ann Surg. 2009; 249: 900-907.
23. Fagotti A, Costantini B, Vizzielli G et al.
HIPEC in recurrent ovarian cancer patients:
morbidity-related treatment and long-term
analysis of clinical outcome. Gynecol Oncol.
2011; 122: 221-225.

136

Huanu I. et al.

Jurnalul de Chirurgie (Iai), 2013, Vol. 9, Nr. 2

24. Gill RS, Al-Adra DP, Nagendran J et al.


Treatment of gastric cancer with peritoneal
carcinomatosis by cytoreductive surgery and
HIPEC: a systematic review of survival,
mortality, and morbidity. J Surg Oncol. 2011;
104: 692-698.
25. Deraco M, Baratti D, Kusamura S. Morbidity
and quality of life following cytoreduction and
HIPEC. Cancer Treat Res. 2007; 134: 403-418.
26. Kerscher AG, Mallalieu J, Pitroff A, Kerscher
F, Esquivel J. Morbidity and mortality of 109
consecutive cytoreductive procedures with
hyperthermic intraperitoneal chemotherapy
(HIPEC) performed at a community hospital.
World J Surg. 2010; 34: 62-69.
27. McQuellon RP, Loggie BW, Fleming RA,
Russell GB, Lehman AB, Rambo TD. Quality
of life after intraperitoneal hyperthermic
chemotherapy
(IPHC)
for
peritoneal
carcinomatosis. Eur J Surg Oncol. 2001; 27:
65-73.
28. Bonastre J, Jan P, de Pouvourville G, Pocard
M, Estphan G, Elias D. [Cost of an
intraperitoneal chemohyperthermia (IPCH)

related to cytoreductive surgery]. Ann Chir.


2005; 130: 553-561.
29. Kilian M, Hammerich R, Langelotz C et al.
[Hyperthermic intraperitoneal chemotherapy
in the German DRG system. Analysis of case
cost calculations of a maximum care
university]. Chirurg. 2005; 81: 1005-1012.
30. Chong GO, Park NY, Hong DG, Cho YL,
Park IS, Lee YS. Learning curve of
laparoscopic radical hysterectomy with pelvic
and/or para-aortic lymphadenectomy in the
early and locally advanced cervical cancer:
comparison of the first 50 and second 50
cases. Int J Gynecol Cancer. 2009; 19: 14591464.
31. Trimbos JB, Hellebrekers BW, Kenter GG,
Peters LA, Zwinderman KH. The long
learning curve of gynaecological cancer
surgery: an argument for centralisation. BJOG.
2000; 107: 19-23.
32. Sarbu V, Maciuceanu B, Supeanu I et al.
[Preliminary results for intraperitoneal
chemotherapy
in
abdominal
cancers].
Chirurgia (Bucureti). 2007; 102: 549-555.

ARTICOLE DE SINTEZ

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STRATEGII TERAPEUTICE N CANCERUL ESOFAGIAN:


ROLUL TRATAMENTULUI CHIRURGICAL
B. Filip, I. Huanu, I. Radu, Maria-Gabriela Aniei, V. Scripcariu
Universitatea de Medicin i Farmacie Gr.T. Popa Iai
Clinica I Chirurgie Oncologic, Institutul Regional de Oncologie Iai
THERAPEUTIC STRATEGIES IN OESOPHAGEAL CANCER: THE PLACE OF
SURGICAL TREATEMENT (Abstract): Any attempt to define the place of surgery in the
treatement of oesophageal cancer should consider the major changes that occurred during the last
two decades: major shift in histologic type, improved staging methods, spectacular reduction of
operative risk, standardization of oncologic principles of resection and the development of
multimodality therapeutic strategies. Surgical treatement plays an essential role in management of
esophageal cancer and it is prefferable to be done by trained surgical teams in large volume
centers. Optimal surgical treatment strategies include appropriate patient selection, accurate
staging, and risk assesment, selection of appropriate surgical approach, and the use of
multimodality treatement.Esophagectomy remaines the main treatement of esophageal carcinoma,
but in half of cases patients are unresectable at the time of diagnosis due to presence of systemic
disease.Two major surgical strategies to improve survival rates after esophagectomy have
emerged during the past decades: limited (transhiatal esophagectomy) and extended
(transthoracic esophagectomy) with two field lymphadenectomy. In the short term, transhiatal
esophagectomy is accompanied by less morbidity, in the long term is preferable for tumors at
gastro-oesophageal junction without involved lymph nodes of chest. For patiets suitable for
surgery, transthoracic esophagectomy with mediastinal and abdominal lymphadenectomy is
preferred. This article provides un up-to-date of options for surgical managing of esophageal
cancer and outlines of surgical technique.
KEY WORDS: ESOPHAGEAL CANCER; SURGERY; LYMPHADENECTOMY; SURVIVAL
SHORT TITLE: Cancerul esofagian rolul tratamentului chirurgical
Esophagian cancer place of surgery
HOW TO CITE:
anu I, Radu I, Aniei MG, Scripcariu V. [Therapeutic strategies in oesophageal cancer: the
place of surgical treatement] Jurnalul de chirurgie (Iai). 2013; 9(2): 137-148. DOI: 10.7438/1584-9341-9-2-4.

INTRODUCERE
Cancerul esofagian (CE) cu 482.300
cazuri noi i 406.800 decese anual ocup
locul 8 ca frecven n lume i reprezint a 6a cauz de deces prin cancer [1].
Majoritatea cancerelor esofagiene sunt
reprezentate de carcinoame scuamocelulare
sau de adenocarcinoame; un numr redus de
cazuri includ leiomiosarcoamele, tumorile
stromale sau tumori nedifereniate.
n zona cu risc maxim, ce se ntinde
din partea nordic a Iranului, trecnd prin
Asia central pn n zona de nord a Chinei,
majoritatea cazurilor sunt reprezentate de

carcinoamele scuamocelulare [2]. Factorii de


risc majori n dezvoltarea acestui tip de
tumor nu sunt complet cunoscui, dar se
crede c statusul nutriional precar,
consumul sczut de fructe i vegetale, i
consumul de buturi alcoolice la temperaturi
crescute ar avea un rol important.
n zonele cu risc scazut, cum ar fi
Europa de Vest i nordul Americii se pare c
fumatul i consumul de alcool sunt ntlnite
la peste 90% din cazurile de cancere
scuamocelulare [3].
Ratele de inciden pentru cele dou
tipuri majore de CE prezint variaii istorice

Received date: 28.02.2013


Accepted date: 10.03.2013
Adresa de coresponden: Dr. Bogdan Filip
Clinica I Chirurgie Oncologic, Institutul Regional de Oncologie Iai
Str. General Henry Mathias Berthlot nr. 2-4, 700483, Iai
Tel.: 0040 (0) 745 25 31 49
E-mail: bfilip79@yahoo.com

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astfel:
incidena
adenocarcinomului
esofagian a crescut n America de Nord i
Europa de Vest odat cu creterea incidenei
obezitii iar incidena carcinomului
scuamocelular a sczut n aceeai zon odat
cu scderea consumului de alcool i a
fumatului. Exist zone din Asia, cum ar fi
Taiwan, n care incidena carcinomului
scuamocelular este n cretere datorit
consumului crescut de alcool i a fumatului
[4].
Carcinomul
scuamocelular
i
adenocarcinomul esofagian reprezint dou
entiti
anatomoclinice
diferite
prin
localizare, factori predispozani, biologie
tumoral i evoluie. Ca i recunoatere a
acestor diferene cea mai nou clasificare
TNM din 2010 separ aceste dou entiti
printr-o stadializare diferit [5].
n practica clinic exist o controvers
privind abordul terapeutic difereniat al
acestor dou entiti anatomoclinice.
Indiferent de tipul histologic, aproximativ
50-60% din pacieni se prezint cu leziuni
local avansate sau metastatice. Prelungirea
supravieuirii este posibil la un numr
limitat de pacieni, pe cnd paliaia
reprezint
tratamentul
ales
pentru
majoritatea acestora. Pentru pacienii cu
leziuni localizate, potenial rezecabile,
supravieuirea median este corelat cu
stadiul tumoral. Doar o minoritate de
pacieni prezint o boal limitat la mucoas
sau submucoas cu o ans de vindecare n
urma tratamentului chirurgical sau, pentru
un subgrup selectat de pacieni, prin rezecie
endoscopic.
Majoritatea pacienilor prezint n
momentul diagnosticului tumori care
invadeaz peretele esofagian (T3) sau au
diseminare limfatic ceea ce limiteaz n
mod considerabil supravieuirea la distan.
Dintre acetia doar 15-20% pot fi vindecai
prin tratamentul multimodal. Tratamentul
optim
pentru
aceti
pacieni
este
controversat, centrele cu experien n
tratamentul CE recomandnd efectuarea
tratamentului
neoadjuvant
chimioradioterpeutic la cei cu tumori peste T2 sau/i
cu diseminare ganglionar la diagnostic.

n virtutea acestor considerente, o


selecie corespunztoare a pacienilor la
tratamentul paliativ, chimio-radioterapic sau
chirurgical este dependent de evaluarea
corect a stadiului tumoral i a
comorbiditilor prezente.
TESTE DIAGNOSTICE
Examenul clinic are valoare limitat n
diagnosticarea n faze potenial curative.
Simptomele
precoce
ale
cancerului
esofagian sunt subtile i nespecifice;
pacientul poate descrie disfagie tranzitorie
pentru alimente solide i care sunt masticate
incomplet,
senzaie
de
discomfort
retrosternal sau de pirozis. Pacienii cu
leziuni local avansate prezint prin
obstrucia mecanic a lumenului esofagian,
disfagie progresiv frecvent asociat cu
scdere ponderal. Disfonia poate fi semnul
unei leziuni local avansate. Tusea recurent
i pneumopatiile recidivante pot fi cauza
unei fistule traheobronice, complicaie
tardiv a CE cauzat de invazia direct a
peretelui posterior traheal sau/i a bronhiei
principale (n general stngi).
Tranzitul
eso-gastro-duodenal
(TEGD) cu substan de contrast poate
sugera diagnosticul de CE. n formele
avansate poate mbrca aspecte caracteristice
de stenoz excentric, nsoit uneori de
dilataia segmentului suprajacent [6]. n
suspiciunile
de
fistul
eso-traheal
(bronic) se recomand utilizarea indexului
opac hidrosolubil de tipul Gastrografin [6].
TEGD permite aprecierea lungimii tumorii,
parametru care este un factor independent de
predicie a supravieuirii [6].
Endoscopia
digestiv
superioar
(EDS) reprezint gold standard n
diagnosticul cancerului esofagian. Dei
vizualizarea endoscopic a unei leziuni
esofagiene poate fi patognomonic pentru
diagnosticul de malignitate, este necesar
documentarea histopatologic prin biopsii
tumorale multiple. Studiile efectuate au
demonstrat c acurateea diagnostic
depinde de numrul de biopsii esofagiene
efectuate: pentru biopsia unic o acurateea
este apreciat la 93%, 3 biopsii de 95% i 7

Cancerul esofagian rolul tratamentului chirurgical

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Jurnalul de Chirurgie (Iai), 2013, Vol. 9, Nr. 2

biopsii de 98% [7]. Asocierea unui periaj


citologic la cele 7 biopsii a crescut
acureteea diagnostic la 100% [7].
Cromoendoscopia, prin colorare cu soluie
Lugol, poate uura identificarea ariei de
biopsiat i are un rol n determinarea
extensiei tumorale, precum i n decelarea
leziunilor sincrone esofagiene [8].
STADIALIZAREA PREOPERATORIE
O corect stadializare preoperatorie
este
esenial
pentru
estimarea
prognosticului maladiei i efectuarea unei
scheme de tratament adecvate. Stadializarea
uzual este TNM a American Joint
Committee on Cancer (AJCC) / International
Union Against Cancer (UICC). Ultima
clasificare din 2010 a introdus o separare a
celor dou tipuri histopatologice majore fa
de clasificarea din 2002, n urma unei
analize de supravieuire a 4627 pacieni cu
cancer de esofag i jonciune gastroesofagian care au urmat doar tratament
chirurgical i la care s-a demonstrat c la
pacienii fr interesare
ganglionar
supravieuirea este direct dependent de
stadiul T, tipul histologic, gradul de
difereniere i localizarea tumoral [9]. Alte
diferene majore fa de clasificarea din
2002 includ: redefinirea tunorilor in situ ca
i displazie de grad nalt, subclasificarea
tumorilor T4 n funcie de rezecabilitatea
structurilor adiacente
invadate, subclasificarea statusului ganglionar n funcie
de numrul de ganglioni regionali invadai,
realocarea n grupe de stadiu utiliznd
categoriile T, N, M ct i gradul de
difereniere histologic, iar pentru tumorile
scuamocelulare funcie de localizarea
tumoral, rencadrarea tumorilor Siewert III
(tumori localizate n primii 5 cm de stomac
cu invazia jonciunii gastro-esofagiene i a
esofagului proximal). Aa cum a fost
menionat aceast nou clasificare a fost
reevaluat utiliznd datele de supravieuire
la pacienii la care nu a fost efectuat un
tratament neoadjuvant, utilitatea acestei
clasificri la pacienii care au efectuat
tratament multimodal este limitat i este
supus verificrii periodice [10,11]. O alt

modificare major a clasificrii din 2010


este legat de definirea adenopatiei locoregionale.
Sunt
considerate
grupe
ganglionare regionale pentru esofagul
toracic: ganglionii periesofagieni superiori
situai cranial de vena azygos, subcarinali i
periesofagieni inferiori situai inferior de
crosa venei azygos; pentru esofagul
abdominal: ganglionii esofagieni inferiori,
diafragmatici, pericardiali, gastrici stngi i
celiaci. Invazia altor grupe ganglionare este
considerat ca metastaz la distan
(ganglionii cervicali sau celiaci pentru
tumorile intratoracice). n noua clasificare se
consider ca factor de prognostic
independent numrul ganglionilor pozitivi.
Examenul computer tomografic (CT)
toraco-abdominal
realizeaz
evaluarea
tumorii primare din punct de vedere al
invazivitii locale i al diseminrii
limfatice, i a diseminrii metastatice. Cu
toate acestea examenul CT are valoare
limitat pentru stadializarea loco-regional,
prin incapacitatea de a prezice cu acuratee
invazia transmural i statusul tumoral al
adenopatiilor [12]. CT are o sensibilitate de
50% i o specificitate de 83% pentru
detectarea
metastazelor
ganglionare
regionale. Pentru metastazele ganglionare
abdominale sensibiliatea i specificitatea CT
este de 42%, respectiv 93%, iar pentru
metastazele la distan de 52%, respectiv
91% [12].
Alt dezavantaj al examenului CT este
capacitatea limitat de a detecta metastazele
de mici dimensiuni (sub 1 cm), lucru care
este evaluat cu acuratee mai mare de ctre
tomografia cu emisie de pozitroni (positron
emission tomography PET) [12].
Explorarea prin rezonan magnetic
nuclear (RMN) nu aduce informaii
suplimentare fa de examenul CT [13].
Dezavantajele utilizrii RMN ar fi costul
crescut i artefactele de micare datorate
respiraiei i contractilitii cardiace.
Specificitatea i sensibiliatea RMN pentru
profunzimea invaziei tumorale este de 40%,
respectiv 63%, iar pentru detectarea
metastazelor ganglionare de 68%, respectiv
62% [13].

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Examenul ecoendoscopic reprezint


cea mai sensibil tehnic imagistic de
evaluare a extensiei locoregionale (Fig. 1),
cu o acuratee pentru categoriile T i N ntre
80 i 90% [14] i ofer o mai bun
stadializare TNM dect CT, imagistica prin
rezonan magnetic (IRM) sau PET, n
special pentru predicia invaziei ganglionare
[15]. Efectuarea punciei cu ac fin a maselor
ganglionare
suspecte
crete
aceast
acuratee. Un inconvenient al acestei
explorri este faptul c transductorul nu
poate depi leziunile stenotice. n aceste
condiii examenul ecoendoscopic poate
substadializa tumora datorit vizualizrii
incomplete a tumorii sau a ganglionilor
periesofagieni. Criteriile ecoendoscopice ale
ganglionilor metastatici sunt dimensiunea
peste 1 cm i aspectul hipoecogen cu
margini slab conturate [16]. Astfel
ecoendoscopia are o acuratee de 80% pentru
caracterizarea
ganglionilor
cervicali
paraesofagieni,
recureniali
drepi,
paratraheali stngi, paraesofageali superiori
i inferiori, infracarinali [14]. Aceast
explorare este folosit pentru restadializarea
pacienilor care au urmat un tratament radiochimioterapic dar cu o acuratee sczut n
caracterizarea rspunsului la neoadjuvan
[17].

Fig. 1 Explorarea ecoendoscopic pentru tumor


esofagian mediotoracic

Tomografia cu emisie de pozitroni (PET)


utilizeaz 18-Fluorodeoxiglucoz reprezint
o metod noninvaziv cu o mai mare

sensibilitate dect CT sau ecoendoscopie


pentru detectarea metastazelor la distan
[12]. Rezultatele studiilor estimeaz c n
20% din cazuri este realizat o stadializare
care schimb indicaia terapeutic i reduce
numrul de pacieni la care este decelat
boala metastatic n momentul interveniei
chirurgicale [18]. Un dezavantaj al explorrii
PET este rezoluia spaial deficitar ce face
dificil localizarea anatomic a captrii 18Fluorodeoxiglucozei. Acest limitare a fost
semnificativ redus prin combinarea PET cu
CT - PET-CT, tehnic n care explorrile
PET i CT sunt efectuate secvenial utiliznd
un scaner hibrid PET/CT. Imaginile obinute
sunt mbinate utiliznd un software specific
permind ca datele fiziologice de la PET s
fie localizate anatomic conform imaginilor
CT (Fig. 2). Msurarea SUV (Standardized
Uptake Value) ce reflect activitatea
metabolic a tumorii poate fi folosit ca
factor prognostic al evoluiei tumorii, o
captare ridicat poate prezice o supravieuire
redus [19]. Evaluarea SUV n momentul
diagnosticului nu a fost demonstrat ca fiind
factor de predicie al rspunsului la
tratamentul neoadjuvant [20,21]. n adiie la
detectarea metastazelor oculte, PET-CT
ofer informaii despre rspunsul metabolic
al tumorii n timpul sau dup tratamentul
neoadjuvant, fapt ce poate fi util n selecia
pacienilor pentru tratamentul chirurgical.
Pentru
a
limita
agresivitatea
tratamentului chirurgical la pacienii cu
boal local avansat a fost propus utilizarea
tehnicilor minim invazive pentru evaluarea
metastazelor peritoneale oculte n special
pentru localizarea esofagian inferioar sau
de jonciune gastro-esofagian [22].
Toracoscopia
i
laparoscopia
diagnostic au fost studiate n scopul
deteciei metastazelor ganglionare celiace i
intratoracice [23]. S-a constatat o
subdiagnosticare a statusului ganglionar prin
CT n 50% din cazuri, prin IRM n 40% i
prin ecoendoscopie n 30% din cazuri
comparativ cu evaluarea toracoscopic sau
laproscopic. Ghidurile NCCN recomand
explorarea laparoscopic opional dac nu
exist eviden de boal metastatic i

Cancerul esofagian rolul tratamentului chirurgical

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Jurnalul de Chirurgie (Iai), 2013, Vol. 9, Nr. 2

tumora este localizat la jonciunea


esogastric
[24].
Adiia
examenului
endoscopic la laparoscopie poate crete
acurateea evalurii locoregionale i
intraperitoneale [25].

Fig. 2 Explorare PET-CT n cadrul unui cancer


scuamocelular mediotoracic

Bronhoscopia este recomandat a se


efectua la pacienii cu boal local avansat
nemetastatic situat la un nivel supracarinal
[26]. Un studiu prospectiv ce a inclus
pacieni candidai la tratament chirurgical a
artat c bronhoscopia poate contraindica
tratamentul chirurgical la 10% din pacieni
[27].
Conform datelor prezentate sunt deci
recomandate ca examene de prim intenie:
1) examenul clinic complet;
2) CT toraco-abdominal;
3) bronhoscopie
pentru
tumorile
esofagului toracic superior i mediu;
4) examen ORL pentru cercetarea unei
paralizii recureniale sau a unui cancer
sincron;
5) CT cerebral sau scintigrafie osoas n
cazul unei simptomatologii sugestive.
Dup excluderea bolii metastatice la
examinrile precedente se asociaz:
1) ecoendoscopia
pentru
aprecierea
gradului de invazie parietal i a
adenopatiilor;
2) ecoendoscopie de nalt frecven
pentru tumori superficiale la care se
intenioneaz rezecie endoscopic,
prin evaluarea cu precizie a
profunzimii extensiei tumorale

Ca i alternative la aceste explorri se


pot folosi: radiografia toracic, ecografia
abdominal, tranzitul baritat esofagian,
ecografia cervical sau supraclavicular,
PET,
laparoscopia
sau
toracoscopia
exploratorie.
Criteriile
absolute
de
nonrezecabilitate sunt:
1) invazia structurilor mediastinale (T4):
arbore traheo-bronic, aort ;
2) Metastaze viscerale sau ganglionare la
distan (M1a, M1b).
Evaluarea strii generale are un rol
important n selectarea pacienilor candidai
la o anumit form de tratament datorit
comorbiditilor prezente n momentul
diagnosticului care pot mpiedica fie
efectuarea tratamentului radio-chimioterapic
fie a celui chirurgical. Aceste explorri
includ: bilan nutriional (procent de scdere
ponderal,
proteinemie,
albuminemie,
prealbuminemie),
evaluarea
statusului
respirator (probe funcionale respiratorii i
gazometrie
sangvin),
cardiovascular
(evaluare clinic, EKG, ecocardiografie),
creatininemie i clearance de creatinin,
bilan hepatic, consiliere privind renunarea
la fumat sau consum de alcool [28].
n urma evalurii statusului general al
pacientului sunt o serie de criterii absolute
de inoperabilitate [28]:
1) insuficiena respiratorie:
- PaO2 < 60 mmHg,
- PaCO2 > 45 mmHg,
- VEMS < 1000 mL/sec,
2) ciroza hepatic decompensat;
3) insuficiena renal (creatinin peste
1,25 valoarea de referin);
4) antecedente
recente
de
infarct
miocardic sau cardiopatie evolutiv.
Contraindicaiile relative sunt [28]:
vrsta peste 75 de ani, scdere ponderal
peste 15%, arteriopatie sever, scor
ECOG > 2.
MODALITI DE TRATAMENT AL CE
Tratamentul chirurgical reprezint
unicul tratament pentru cancerele precoce
(T1-2N0) sau ca asociere la tratamentul radio-

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chimioterapic pentru leziunile local avansate


(T3, T1-2N+) [24,29].
Pentru tumorile in situ se practic
mucosectomia endoscopic cu controlul
histopatologic atent al marginilor de rezecie
[24,29].
Tehnicile chirurgicale utilizate difer
n funcie de sediul anatomic al leziunii,
statusul general al pacientului, tipul de
limfadenectomie ales i de experiena
echipei chirurgicale. Vom descrie pe scurt
tehnicile chirurgicale cel mai frecvent
utilizate n tratamentul cancerului esofagian
i de jonciune gastroesofagian fr a intra
n detalii de tehnic chirurgical.
Pacienii cu adenocarcinom sau cancer
scuamocelular localizat la nivelul esofagului
toracic mediu sau inferior beneficiaz de
esofagectomie total n principal datorit
riscului de leziuni sincrone mucoase sau
skip-lesions submocoase [30]. Dac este
efectuat o esofagectomie subtotal este
obligatorie evaluarea extemporanee a
marginilor de rezecie.
Esofagectomia transhiatal, IvorLewis (transtoracic) sau triplul abord
(McKeown) sunt cele mai utilizate tehnici n
America de Nord i Europa, pe cnd
esofagectomia cu triplu chiuraj ganglionar
este preferat n rile asiatice [31].
Grefonul esofagian cel mai utilizat este
reprezentat de stomac, dar poate fi folosit
colonul sau jejunul [32,33]. Utilizarea
acestor dou din urm impun efectuarea a
dou anastomoze suplimentare [34].
Esogafectomia transhiatal poate fi
utilizat pentru toate localizrile neoplazice
printr-o laparotomie median i o incizie
cervical, cu disecie boant esofagian i
crearea unei anastomoze cervicale [35].
Dezavantajul major este reprezentat de
incapacitatea efecturii unui chiuraj ganglionar
mediastinal. Cea mai larg serie de pacieni la
care s-a practicat aceast tehnic raporteaz o
mortalitate de 4% i fistule cervicale de 13%
[36]. Alte complicaii descrise sunt paralizia
recurenial, chylotoraxul, leziunile traheale
[36].

Esofagectomia Ivor-Lewis poate fi


utilizat n tratamentul CE de treime
inferioar i combin o laparotomie median
cu o toracotomie dreapt (Fig. 3) i
anastomoz intratoracic eso-gastric, ceea
ce permite o limfadenectomie direct toracoabdominal. Dezavantajele acestei tehnici
sunt capacitatea limitat de a oferi un
clearance esofagian n limite de siguran
oncologic,
localizarea
toracic
a
anastomozei i riscul crescut de reflux biliar
[37]. Apariia unei fistule la nivel toracic
duce la un risc crescut de morbiditate i
mortalitate [38].
Studiile prospective [39,40] precum i
rezultatul
unei
meta-analize
[41]
demonstreaz
supravieuire
similar
comparativ cu tehnicile transhiatale.

Fig. 3 Disecia esofagului prin toracotomie dreapt

O modificare a tehnicii Ivor-Lewis ce


include o incizie toraco-abdominal stng
cu rezecie esofagogastric parial i
anastomoz esogastric intratoracic sub
arcul aortic [42] poate fi utilizat ca
alternativ pentru tumorile de jonciune esogastric.
Esofagectomia prin triplu abord, ca i
combinaie a celor dou tehnici descrise mai
sus, permite o esofagectomie total prin
abord toracic, abdominal cu anastomoz
cervical [43,44].
Acest tip de abord permite efectuarea
unei limfadenectomii complete abdominale
i toracice.

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Abordul toracic ca prim timp operator


permite
evaluarea
rezecabilitii
i
efectuarea rezeciei i limfadenectomiei
mediastinale, fiind urmat de timpul
abdominal ce exclude boala metastatic i
permite mobilizarea stomacului cu crearea
grefonului de substituie i limfadenectomia
pe cmpul abdominal. Timpul final este
reprezentat de incizia cervical stng ce
permite transecia esofagului i exizia piesei
de rezecie la nivel abdominal cu
ascensionarea grefonului i anastomoza la
acest
nivel. Avantajele anastomozei
cervicale sunt reprezentate de managementul
mai facil al unei complicaii fistulare,
incidena sczut a refluxului biliar i
plasarea anastomozei n afara cmpului de
iradiere toracic.
Cancerele localizate la nivelul
jonciunii esogastrice pot fi tratate prin abord
toraco-abdominal, gradul de rezecie gastric
fiind dictat de extensia la nivelul polului
superior gastric, sau prin tehnici transhiatale.
Un studiu randomizat de faz III a analizat
rezultatele postoperatorii la pacienii cu
tumori de jonciune gastroesofagian
Siewert I sau II la care s-au aplicat tenhici
transhiatale sau transtoracice [45]. Nu au
fost diferene din punct de vedere al
mortalitii postoperatorii, dar complicaiile
pulmonare i fistula de duct toracic au fost
mai frecvente dup tehnicile transtoracice.
De asemenea, durata de spitalizare n secia
de terapie intensiv i durata total de
spitalizare a fost mai mare la aceti pacieni.
Nu au fost observate diferene din punct de
vedere al supravieuirii la 5 ani.
Tehnicile minim-inavzive au ca avantaj
inciziile parietale minime, pierderile sczute
de snge, rata sczut de complicaii n
special cardio-pulmonare, durata sczut de
spitalizare [46].
O meta-analiz a 12 studii ce au inclus
pacieni cu esofagectomie minim-invaziv
sau hibrid nu a artat diferene privind
mortalitatea la 30 de zile [47].
Cu toate c nu au fost diferene n ceea
ce privete incidena fistulelor anastomotice,
pacienii cu tehnici minim-invazive hibride

au prezentat mai puine complicaii fistulare


(OR: 0,51; 95% CI 0,28-0,91).
Tehnicile minim-invazive (Fig. 4) au
fost asociate cu pierderi sczute de snge,
rat sczut de complicatii pulmonare, cu o
reducere global de morbiditate de 50%
[47]. Tehnicile hibride au prezentat aceeai
rat de morbiditate ca i chirurgia deschis
prin
pstrarea
toracotomiei
sau
a
laparotomiei ca i factor de risc.

Fig. 4 Aspect final al unei esofagectomii prin abord


toracoscopic

Pn n prezent nu exist un consens


privind extensia limfadenectomiei n CE.
Examinarea a minim 6 ganglioni
mediastinali este necesar pentru o evaluare
corect a statusului ganglionar toracic i se
recomand rezecia a minim 15 ganglioni
(abdominali i toracici).
Tehnica cea mai utilizat este
limfadenectomia pe dou cmpuri (toracic i
abdominal) ce este asociat cu cel mai bun
control loco-regional. Tehnicile extensive ce
asociaz limfadenectomia cervical sunt larg
utilizate n rile asiatice pentru tumori
esofagiene cervicale i de treime superioar
[48]. Cel puin dou studii randomizate au
comparat beneficiile diferitelor tipuri de
limfadenectomie n tratamentul cancerului
esofagian i nu au demonstrat beneficii ale
tehnicilor extensive [45,49].
Rezultate tardive dup tratamentul
chirurgical difer n funcie de nivelul de
expertiz al centrului chirurgical.
Supravieuirea medie la 5 ani este de
30% pe serii multicentrice [50] i de 40% dac
sunt incluse doar centrele cu experien [51].

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RADIOTERAPIA I CHIMIOTERAPIA
Tratamentul
definitiv
radiochimoterapic este adresat cancerelor nonoperabile sau non-rezecabile nemetastatice.
n cazul asocierii radio-chimioterapice doza
total a radioterapiei este recomandat a fi
de 50 Gy, o doz mai mare nu amelioreaz
supravieuirea [52]. Radioterapia exclusiv
poate fi luat n considerare la pacienii la
care exist contraindicaii clare pentru
tratamentul chimioterapic [24]. Tratamentul
brahiterapic se poate utiliza ca i modalitate
de
dezobstrucie
esofagian
pentru
tratamentul paliativ al disfagiei [24].
Asocierea
radiochimioterapiei
i
chirurgiei face parte din tratamentul
multimodal al cancerului esofagian i este
adresat tumorilor local avansate cu invazie
ganglionar n momentul diagnosticului
pentru ca s-a observat c prin aplicarea
acestui protocol de neoadjuvan sunt
obinute cele mai bune rezultate la distan
[53,54].
Conceptul de salvage surgery este
aplicat n cazurile absenei rspunsului la
tratamentul neoadjuvant radio/chimioterapic.
Pn n prezent nu sunt studii randomizate
care s valideze beneficiile acestui concept
n cancerul esofagian. Un studiu a
demonstrat o supravieuire de 32% la 3 ani
la cei care nu au avut un rspuns la
tratamentul neoadjuvant i care au
beneficiat de rezecii R0, ajungnd la 50% la
cei care au rspuns la tratament [55]. ntr-o
serie de 98 de tumori subcarinale care nu au
rspuns la neoadjuvan, o rezecie R0 a fost
realizat la 62% cu o supravieuire median
de 18,4 luni [56]. Acest concept de salvage
surgery trebuie aplicat cu discernmnt dup
evaluarea n echip multidisciplinar a
fiecrui caz.
Chimioterapia paliativ n cancerele
metastatice ce include Cisplatin i 5Fluorouracil nu a demonstrat a avea efecte
de prelungire a supravieuirii comparativ cu
tratamentul simptomatic. Aceast asociere
poate duce la obinerea n 30-40% din cazuri
a unui rspuns obiectiv cu o durat median
de supravieuire de 8-12 luni. Asocierea de
Irinotecan-Cisplatin, Gemcitabin-Cisplatin,

Vinorlebin-Cisplatin
sau
PaclitaxelCisplatin poate obine un rspuns ntre 3060% [57-59].
Chimioterapia
neoadjuvant
a
demonstrat beneficii de supravieuire (3.5
luni de supravieuire median i un plus de
9% de supravieuire la 2 ani) prin precedarea
tratamentului chirurgical cu 2 cure de
Cisplatin i 5-Fluorouracil [60]. Acest
tratament nu a crescut mortalitatea
postoperatorie i a devenit tratamentul de
referin pentru adenocarcinomele de
jonciune gastro-esofagian i ca alternativ
pentru tumorile scuamocelulare [60].
Tratamentele endoscopice cu viz
curativ se adreseaz tumorilor superficiale
m1 sau m2 diagnosticate ecoendoscopic.
Mucosectomia endoscopic este tratamentul
recomandat, avantajul major fa de alte
metode de distrucie local (laser,
fototerapie, brahiterapie) fiind posibilitatea
efecturii examenului histopatologic [24].
Tehnicile endoscopice cu viz paliativ
includ: dilataii esofagiene, endoprotezarea,
citoreducia tumoral, scopul principal fiind
ameliorarea disfagiei [24].
INDICAII TERAPEUTICE
1) cancerele superficiale (Tis, T1-m1 sau
T1-m2) - tratament endoscopic de prim
intenie, ca i alternativ se poate alege
ntre
esofagectomie,
radiochimioterapie, radioterapie, fototerapie
dinamic, distrucie cu laser [24];
2) cancere invazive operabile:
a) T1-2N0: tratamentul de referin este
esofagectomia, ca i alternativ se
radiochimioterapia
exclusiv
(cancer
epidermoid
cervical)
[24,61,62];
b) T1N1, T2N1, T3N0: se recomand
tratament
neoadjuvant
radiochimioterapic urmat de reevaluare
n vederea esofagectomiei [24,62].
Tratamentul
radio-chimioterapic
definitiv este folosit la pacienii ce
au contra indicaii generale de
intervenie chirurgical sau dezvolt
boal
metastatic
n
cursul
tratamentului neoadjuvant.

Cancerul esofagian rolul tratamentului chirurgical

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Jurnalul de Chirurgie (Iai), 2013, Vol. 9, Nr. 2

c) T3N1, T4aN0-1: se recoman


efectuarea
radiochimioterapiei
neoadjuvante [24,62] i evaluarea
rspunsului la tratamen. Stabilirea
indicaiei terapeutice este efectuat
dup evaluare multidisciplinar
[24,62].
3) cancerele esofagului cervical: nu exist
un tratament de referin; cum n
majoritatea cazurilor sunt carcinomae
epidermoide,
radiochimioterapia
definitiv
este
soluia
optim.
Stabilirea indicaiei chirurgicale se
face doar dup o reevaluare complet a
cazului. [24,62]
4) cancere inoperabile non metastatice
T4a [24,62]:
a) fr
invazie
traheobronic:
radiochimioterapie definitiv;
b) cu
invazie
traheobronic:
chimioterapie urmat de radiochimioterapie n cazul dispariiei
invaziei bronice sau tratament
endoscopic;
c) cu fistul esotraheal: nu exist un
consens. Stabilirea indicaiei de
tratament este individual dup
evaluarea cazului n cadrul comisiei
multidisciplinare.
5) cancere
metastatice:
obiectivul
principal
este
prelungirea
supravieuirii i ameliorarea calitii
vieii: tratament endoscopic al
disfagiei
cu
sau
fr
radiochimioterapie [24,62].
CONCLUZII
Definirea
rolului
tratamentului
chirurgical n cancerul esofagian rmne o
problem de interes datorit schimbrilor
majore n incidena subtipurilor histologice
i a noilor metode de stadializare
preoperatorie. A fost conturat necesitatea
efecturii tratamentului neoadjuvant la
pacienii cu tumori local avansate, n acest
caz tratamentul chirurgical fiind adresat i
avnd cele mai bune rezultate la pacienii
considerai a avea un rspuns cuantificabil la
tratament. Avnd n vedere experiena
cazurilor de cancer esofagian din Romnia,

marea majoritate fiind diagnosticate n faze


local avansate, suntem n favoarea
tratamentului neoadjuvant urmat, n cazul
rspunsului la tratament, de intervenia
chirurgical.
CONFLICT DE INTERESE
Autorii nu declar nici un conflict de
interese.

BIBLIOGRAFIE
1. Jemal A, Bray F, Center Mm, et al. Global
cancer statistics. CA Cancer J Clin. 2011;
61(2): 69-90.
2. Gholipour C, Shalchi RA, Abbasi M. A
histopathological study of esophageal cancer
on the western side of the Caspian littoral from
1994 to 2003. Dis Esophagus. 2008; 21(4):
322-327.
3. Engel LS, Chow WH, Vaughan TL, et al.
Population attributable risks of esophageal and
gastric cancers. J Natl Cancer Inst. 2003;
95(18): 1404-1413
4. Lu CL, Lang HC, Luo JC, et al. Increasing
trend of the incidence of esophageal squamous
cell carcinoma, but not adenocarcinoma, in
Taiwan. Cancer Causes Control. 2010; 21(2):
269-274.
5. Edge SB, Byrd DR, Compton CC, et al.
American Joint Committee on Cancer Staging
Manual, 7th edition, New York: Springer,
2010. p. 103.
6. Yendamuri S, Swisher SG, Correa AM, et al.
Esophageal tumor length is independently
associated with long-term survival. Cancer.
2009; 115(3): 508-516.
7. Graham DY, Schwartz JT, Cain GD, et al.
1982. Prospective evaluation of biopsy
number in the diagnosis of esophageal and
gastric carcinoma. Gastroenterology. 1982;
82(2): 228-231.
8. Acosta
MM,
Boyce
HW
Jr.
Chromoendoscopy--where is it useful? J Clin
Gastroenterol. 1998; 27(1): 13-20.
9. Rice TW, Rusch VW, Ishwaran H, et al.
Cancer of the esophagus and esophagogastric
junction: data-driven staging for the seventh
edition of the American Joint Committee on
Cancer/International Union Against Cancer
Cancer Staging Manuals. Cancer. 2010;
116(16): 3763-3773.
10. Barbour AP, Jones M, Gonen M, et al.
Refining esophageal cancer staging after
neoadjuvant therapy: importance of treatment
response. Ann Surg Oncol. 2008; 15(10):
2894-2902.

146

Filip B. et al.

Jurnalul de Chirurgie (Iai), 2013, Vol. 9, Nr. 2

11. Rizk NP, Venkatraman E, Bains MS, et al.


American Joint Committee on Cancer staging
system does not accurately predict survival in
patients receiving multimodality therapy for
esophageal adenocarcinoma. J Clin Oncol.
2007; 25(5): 507-512.
12. van Vliet EP, Heijenbrok-Kal MH, Hunink
MG, et al. Staging investigations for
oesophageal cancer: a meta-analysis. Br J
Cancer. 2008; 98(3): 547-557.
13. Wu LF, Wang BZ, Fenq JL, et al. Preoperative
TN staging of esophageal cancer : comparison
of miniprobe ultrasonography, spirat CT and
MRI. World J Gatroenterol. 2003; 9(2): 219224.
14. Chandawarkar RY, Kakegawa T, Fujita H, et
al. Endosonography for preoperative staging
of specific nodal groups associated with
esophageal cancer. World J Surg. 1996; 20(6):
700-702.
15. Keswani RN, Early DS, Edmundowicz SA, et
al. Routine positron emission tomography
does not alter nodal staging in patients
undergoing EUS-guided FNA for esophageal
cancer. Gastrointest Endosc. 1996; 20(6): 700702.
16. Brugge WR, Lee MJ, Carey RW, et al.
Endoscopic ultrasound staging criteria for
esophageal cancer. Gastrointest Endosc. 1997;
45(2): 147-152.
17. Schneider PM, Metzger R, Schaefer H, et al.
Response evaluation by endoscopy, rebiopsy,
and endoscopic ultrasound does not accurately
predict histopathologic regression after
neoadjuvant chemoradiation for esophageal
cancer. Ann Surg. 2008; 248(6): 902-908.
18. van Westreenen HL, Heeren PA, van
Dullemen HM, et al. Positron emission
tomography with F-18-fluorodeoxyglucose in
a combined staging strategy of esophageal
cancer
prevents
unnecessary
surgical
explorations. J Gastrointest Surg. 2005; 9(1):
54-61.
19. Erasmus JJ, Munden RF. The role of
integrated computed tomography positronemission tomography in esophageal cancer:
staging and assessment of therapeutic
response. Semin Radiat Oncol. 2007; 17(1):
29-37.
20. Meyers BF, Downey RJ, Decker PA, et al. The
utility of positron emission tomography in
staging of potentially operable carcinoma of
the thoracic esophagus: results of the
American College of Surgeons Oncology
Group Z0060 trial. J Thorac Cardiovasc Surg.
2007; 133(3): 738-745.
21. Kwee RM. Prediction of tumor response to
neoadjuvant therapy in patients with
esophageal cancer with use of 18F FDG PET:

a systematic review. Radiology. 2010; 254(3):


707-717.
22. Kaushik N, Khalid A, Brody D, et al.
Endoscopic ultrasound compared with
laparoscopy for staging esophageal cancer.
Ann Thorac Surg. 2007; 83(6): 2000-2002.
23. Krasna MJ, Reed CE, Nedzwiecki D, et al.
CALGB 9380: a prospective trial of the
feasibility of thoracoscopy/laparoscopy in
staging esophageal cancer. Ann Thorac Surg.
2001; 71(4): 1073-1079.
24. National Comprehensive Cancer Network
(NCCN)
guidelines.
Available
at:
www.nccn.org
25. Wakelin SJ, Deans C, Crofts TJ, et al. A
comparison of computerised tomography,
laparoscopic ultrasound and endoscopic
ultrasound in the preoperative staging of
oesophago-gastric carcinoma. Eur J Radiol.
2002; 41(2): 161-167.
26. Riedel M, Stein HJ, Mounyam L, et al.
Extensive sampling improves preoperative
bronchoscopic assessment of airway invasion
by supracarinal esophageal cancer: a
prospective study in 166 patients. Chest. 2001;
119(6): 1652-1660.
27. Riedel M, Hauck RW, Stein HJ, et al.
Preoperative bronchoscopic assessment of
airway invasion by esophageal cancer: a
prospective study. Chest. 2001; 119(6): 16521660.
28. Congedo E, Aceto P, Petrucci R, et al.
Preoperative anesthetic evaluation and
preparation in patients requiring esophageal
surgery for cancer. Rays. 2005; 30(4): 341345.
29. Fumagalli U and Panel of experts. Resective
surgery for cancer of the thoracic esophagus.
Results of a Consensus Conference at the VIth
World Congress of the International Society
for Diseases of the Esophagus. Dis Esoph.
1996; 9(Suppl 1): 30-38.
30. Kato H, Tachimori Y, Watanabe H, et al.
Intramural metastasis of thoracic esophageal
carcinoma. Int J Cancer. 1992; 50(1): 49-52.
31. Tachibana M, Kinugasa S, Yoshimura H, et al.
Clinical outcomes of extended esophagectomy
with three-field lymph node dissection for
esophageal squamous cell carcinoma. Am J
Surg. 2005; 189(1): 98-109.
32. Davis PA, Law S, Wong J. Colonic
interposition after esophagectomy for cancer.
Arch Surg. 2003; 138(3): 303-308.
33. Mansour KA, Bryan FC, Carlson GW. Bowel
interposition for esophageal replacement:
twenty-five-year experience. Ann Thorac
Surg. 1997; 64(3): 752-756.
34. Cordos I. Resection and reconstruction of the
esophagus with a triple approach: thoracic,

Cancerul esofagian rolul tratamentului chirurgical

147
Jurnalul de Chirurgie (Iai), 2013, Vol. 9, Nr. 2

abdominal, cervical. Chirurgia (Bucureti).


2006; 101: 519-522.
35. Ellis FH Jr., Gibb SP, Watkins E Jr.
Esophagogastrectomy.
A safe,
widely
applicable, and expeditious form of palliation
for patients with carcinoma of the esophagus
and cardia. Ann Surg. 1983; 198(4): 531-540.
36. Orringer MB, Marshall B, Iannettoni MD.
Transhiatal
esophagectomy:
clinical
experience and refinements. Ann Surg. 1999;
230: 392-400.
37. Baba M, Aikou T, Natsugoe S, et al. Appraisal
of ten-year survival following esophagectomy
for carcinoma of the esophagus with emphasis
on quality of life. World J Surg. 1997; 21:
282-285.
38. Urschel
JD.
Esophago-gastrostomy
anastomotic
leaks
complicating
esophagectomy: a review. Am J Surg. 1995;
169: 634-640.
39. Omloo JM, Lagarde SM, Hulscher JB, et al.
Extended transthoracic resection compared
with limited transhiatal resection for
adenocarcinoma of the mid/distal esophagus:
five-year survival of a randomized clinical
trial. Ann Surg. 2007; 246(6): 992-1000.
40. Rentz J, Bull D, Harpole D, et al.
Transthoracic
versus
transhiatal
esophagectomy: a prospective study of 945
patients. J Thorac Cardiovasc Surg. 2003;
125(5): 1114-11120.
41. Hulscher JB, Tijssen JG, Obertop H, et al.
Transthoracic versus transhiatal resection for
carcinoma of the esophagus: a meta-analysis.
Ann Thorac Surg. 2001; 72(1): 306-313.
42. Krasna MJ. Left transthoracic esophagectomy.
Chest Surg Clin N Am. 1995; 5: 543-554
43. Swanson SJ, Batirel HF, Bueno R, et al.
Transthoracic esophagectomy with radical
mediastinal and abdominal lymph node
dissection and cervical esophagogastrostomy
for esophageal carcinoma. Ann Thorac Surg.
2001; 72(6): 1918-1924.
44. McKeown KC. The surgical treatment of
carcinoma of the oesophagus. A review of the
results in 478 cases. J R Coll Surg Edinb.
1985; 30: 1-14.
45. Hulscher JB, van Sandick JW, de Boer AG, et
al. Extended transthoracic resection compared
with limited transhiatal resection for
adenocarcinoma of the esophagus. N Engl J
Med. 2002; 347(21): 1662-1669.
46. Biere SS, van Berge Henegouwen MI, Maas
Kw, et al. Minimally invasive versus open
oesophagectomy for patients with oesophageal
cancer: a multicentre, open-label, randomised
controlled trial. Lancet. 2012; 379(9829):
1887-1892.
47. Nagpal K, Ahmed K, Vats A, et al. Is
minimally invasive surgery beneficial in the

management of esophageal cancer? A metaanalysis. Surg Endosc. 2010; 24(7): 16211629.


48. Li B, Chen H, Xiang J, et al. Pattern of
lymphatic spread in thoracic esophageal
squamous cell carcinoma: A single-institution
experience. J Thorac Cardiovasc Surg. 2012;
144(4): 778-785.
49. Nishihira T, Hirayama K, Mori S. A
prospective randomized trial of extended
cervical
and
superior
mediastinal
lymphadenectomy for carcinoma of the
thoracic esophagus. Am J Surg. 1998; 175(1):
47-51.
50. Bouvier AM, Binquet C, Gagnaire A, et al.
Management and prognosis of esophageal
cancers: has progress been made? Eur J
Cancer. 2006; 42(2): 228-233.
51. Mariette C, Piessen G, Balon JM, et al.
Surgery alone in the curative treatment of
localised oesophageal carcinoma. Eur J Surg
Oncol. 2004; 30(8): 869-876.
52. Minsky BD, Pajak TF, Ginsberg RJ, et al. INT
0123 (Radiation Therapy Oncology Group 9405) phase III trial of combined-modality
therapy for esophageal cancer: high-dose
versus standard-dose radiation therapy. J Clin
Oncol. 2002; 20(5): 1167-1174.
53. Urschel JD, Vasan H. A meta-analysis of
randomized controlled trials that compared
neoadjuvant chemoradiation and surgery to
surgery alone for resectable esophageal
cancer. Am J Surg. 2003; 185(6): 538-543.
54. Burmeister BH, Smithers BM, Gebski Vet al.
Surgery alone versus chemoradiotherapy
followed by surgery for resectable cancer of
the oesophagus: a randomised controlled phase
III trial. Lancet Oncol. 2005; 6(9): 659-668.
55. Stahl M, Stuschke M, Lehmann N, et al.
Chemoradiation with and without surgery in
patients with locally advanced squamous cell
carcinoma of the esophagus. J Clin Oncol.
2005; 23(10): 2310-2317.
56. Piessen G, Briez N, Triboulet JP, et al.
Patients with locally advanced esophageal
carcinoma
nonresponder
to
radiochemotherapy: who will benefit from surgery?
Ann Surg Oncol. 2007; 14(7): 2036-2044.
57. Conroy T, Etienne PL, Adenis A, et al.
Vinorelbine and cisplatin in metastatic
squamous cell carcinoma of the oesophagus:
response, toxicity, quality of life and survival.
Ann Oncol. 2002; 13(5): 721-729.
58. Kroep JR, Pinedo HM, Giaccone G, et al.
Phase II study of cisplatin preceding
gemcitabine in patients with advanced
oesophageal cancer. Ann Oncol. 2004; 15(2):
230-235.
59. Assersohn L, Brown G, Cunningham D, et al.
Phase II study of irinotecan and 5-

148

Filip B. et al.

Jurnalul de Chirurgie (Iai), 2013, Vol. 9, Nr. 2

fluorouracil/leucovorin in patients with


primary refractory or relapsed advanced
oesophageal and gastric carcinoma. Ann
Oncol. 2004; 15(1): 64-69.
60. Medical Research Council Oesophageal
Cancer Working party. Surgical resection with
or without preoperative chemotherapy in

oesophageal cancer : a randomised controlled


trial. Lancet. 2002; 359(9319): 1727-1733.
61. Rice TW, Mason DP, Murthy SC, et al.
T2N0M0 esophageal cancer. J Thorac
Cardiovasc Surg. 2007; 133(2): 317-324.
62. Cancer de loesophage. Referentiel Nord Pas
de Calais. Available at www.onco-npdc.fr.

ORIGINAL ARTICLE

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INTRAOPERATIVE DIFFICULTIES IN LAPAROSCOPIC


CHOLECYSTECTOMY
S.K. Sahu , A. Agrawal, P.K. Sachan
Department of General Surgery, Himalayan Institute of Medical Sciences
INTRAOPERATIVE DIFFICULTIES IN LAPAROSCOPIC CHOLECYSTECTOMY
(Abstract): INTRODUCTION: Laparoscopic surgery has certain technical limitations like loss of
three-dimensional perception, a relatively limited and fixed view of operative field, indirect
contact with intraabdominal structures, and limited tactile feedback during dissection and
manipulation of tissues. This makes operation difficult sometimes and leads to conversion to open
cholecystectomy. AIM: The aim of the study was to study the intraoperative difficulties in
Laparoscopic Cholecystectomy. MATERIAL AND METHODS: This is a prospective study over
a period of 12 months in the Department of General Surgery at Himalayan Institute of Medical
Sciences, HIHT University, Dehradun, Uttarakhand, India. Difficult Laparoscopic
Cholecystectomy was defined in those procedures which exceeded 90 minutes in duration and or
converted to open procedure. Per operative difficulties were classified and studied in the
following steps during the procedure: 1) Creation of the pneumoperitoneum; 2) Separation of all
adhesions; 3) Skeletonization, ligation and division of cystic artery and cystic duct; 4) Excision of
Gall Bladder from the gall bladder fossa of the liver bed; 5) Extraction of Gall Bladder. RESULT:
200 patients who underwent Laparoscopic Cholecystectomy presenting to our hospital from
March 2011 to February 2012 were included in this study. Out of 200 laparoscopic
cholecystectomy (LC) 130 (65%) were easy and 70 (35%) were difficult. Out of these 70 difficult
cases 12 (6%) required conversion to open cholecystectomy. The conversion rate was higher in
the age group of > 60 years. The maximum difficulty occurred while separating the adhesions
75.71% out of 70 cases. Maximum difficulty while performing this step of LC was found in
patients with Previous Abdominal Surgery 8 (50%). Maximum number of adhesions and
difficulty separating them was seen in patients with acute cholecystitis 22 (41.50%). Out of 70
difficult cases there were 39 (55.71%) cases in which skeletonization, ligation and division of
cystic artery and duct was difficult. Maximum difficulty in this step of LC was seen in patients
with abnormal callots anatomy 20 (51.28 %). Maximum conversion rate was seen with patients
having abnormal callots anatomy 35%. CONCLUSIONS : Previous abdominal surgery,
intrahepatic gallbladder, multiple large calculi, very thick walled gallbladder, acute cholecystitis
and abnormal callots anatomy are the difficult factors to operate upon and increases the operating
time. Acute cholecystitis and abnormal callots anatomy are the two conditions in which the
conversion rate is higher.
KEY
WORDS:
GALL BLADDER;
LAPAROSCOPIC
SURGERY;
LAPAROSCOPIC CHOLECYSTECTOMY; CALOTS TRIANGLE

DIFFICULT

SHORT TITLE: Difficulties in laparoscopic cholecystectomy


HOW TO CITE: Sahu SK, Agrawal A, Sachan PK. Intraoperative difficulties in laparoscopic cholecystectomy. Jurnalul
de chirurgie (Iai). 2013; 9(2): 149-155. DOI: 10.7438/1584-9341-9-2-5.

INTRODUCTION
The first laparoscopic cholecystectomy
(LC) using keyhole approach was done by
Professor Mouret of Lyon, France in 1987,

when he was completing a gynaecologic


laparoscopy on a woman also suffering from
symptomatic gall stones, he removed it
laparoscopically instead of opening up.

Received date: 28.02.2013


Accepted date: 20.03.2013
Correspondence to: Shantanu Kumar Sahu, MS, FAIS, FMAS, FIAGES.
Department of General Surgery Himalayan Institute of Medical Sciences
Swami Ram Nagar Post - Doiwala Dehradun Uttarakhand, India, Pin 248140;
Phone: 0091 (0) 9412 93 38 68
Fax: 0091 (0) 1352 47 13 17
E-mail: lntshantanu@yahoo.co.in

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Dr. Eddie Reddick reported 100 cases


of laparoscopic cholecystectomy in 1989.
The classical four port technique of LC as
described by Reddick became the most
widely adopted technique. LC was
considered by most to be at its zenith since
its inception in the early 1990s and is also
now done by 2 and 3 ports. When LC was
started, only simple gall stone disease was
considered as indication. With increasing
expertise and introduction of newer
instruments, acute cholecystitis has also
become one of the indications for LC. Now
any type of calculus cholecystitis can be
managed by laparoscopic method. The skill
of the surgeon, experience in laparoscopic
techniques and thorough knowledge of the
risk factors are important for laparoscopic
management of gall stone disease in
difficult situation without increasing the
morbidity. [1]
Laparoscopic surgery has certain
technical limitations like loss of threedimensional perception, a relatively limited
and fixed view of operative field, indirect
contact with intraabdominal structures, and
limited tactile feedback during dissection
and manipulation of tissues. This makes
operation difficult sometimes and leads to
conversion to open cholecystectomy. The
definition
of
difficult
laparoscopic
cholecystectomy (LC) is inconsistent. The
term difficult cholecystectomy refers to
multiple technical intra-operative difficulties
that increases the risk complications and
significantly prolongs operation time. [2, 3]
The aim of the study was to study the
intraoperative difficulties in LC.
MATERIAL AND METHODS
This study was carried out over a
period of 12 months prospectively in the
Department of General Surgery at
Himalayan Institute of Medical Sciences,
HIHT University, Dehradun, Uttarakhand,
India. All the patients who underwent LC
presenting to our hospital were included in
this study. A sample size of 200 was
included in the study. Exclusion criteria
includes preoperatively proven gall bladder

malignancy, refractory coagulopathy, severe


cardio-pulmonary disease, as these patients
cannot tolerate CO2 pneumoperitoneum and
patients unfit for general anaesthesia due to
any other reason. Total duration of surgery
from the insertion of veress needle to the
closure of port site and conversion to open
cholecystectomy, if any and the cause of
conversion were also studied. Surgeons with
experience of more than 100 laparoscopic
cholecystectomies did all the surgeries in
this study.
Difficult LC was defined in those
procedures which exceeded 90 minutes in
duration and or converted to open procedure.
Per operative difficulties were
classified and studied in the following steps
during the procedure:
1) Creation of the pneumoperitoneum;
2) Separation of all adhesions;
3) Skeletonization, ligation and division
of cystic artery and cystic duct;
4) Excision of gall bladder (GB) from the
gall bladder fossa of the liver bed;
5) Extraction of GB.
Overlapping of these intra operative
difficulties were recorded and considered
while doing the statistical analysis. The data
collected was represented in the form of bar
diagram and pie diagrams. The results have
been analysed by using unpaired t-test.
RESULTS
This study was carried out over a
period of 12 months from March 2011 to
February 2012, prospectively in the
Department of General Surgery at
Himalayan Institute of Medical Sciences,
HIHT University, Dehradun, Uttarakhand,
India. 200 patients who underwent LC
presenting to our hospital were included in
this study.
Out of 200 LC, 130 (65%) were easy
and 70 (35%) were considered as difficult.
Out of these 70 difficult cases 12
(6%) required conversion to open
cholecystectomy.
All those cases which were converted
from laparoscopic to open cholecystectomy
were included in the difficult laparoscpic

Difficulties in laparoscopic cholecystectomy

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entity irrespective of
conversion (Table I, II).

the

timing

of

Table I Duration of surgery (n=200)


Time (mins)

n (%)

Male

Female

31 - 60

60 (30%)

14

46

61 - 90

70 (35%)

19

51

> 91

58 (29%)

20

38

Conversions

12 (6%)

< 30

difficulty while performing this step of LC


was found in patients with Previous
Abdominal Surgery 8 (50%) (Table III).
There were 53 (75.71%) patients
who had difficulty in separating adhesions
(Fig. 2). Maximum number of adhesions and
difficulty separating them was seen in
patients with acute cholecystitis 22 (41.50%)
(Table IV).
Fig. 2 Difficult spectrum

Table II Laparoscopic cholecystectomy group (n=200)


Time

Percentage

Difficult as per timing

58

29%

Conversion

12

6%

Easy

130

65%

The conversion was also seen highest


in the age group of > 60 years. In females 3
(1.5%) and among males the conversion was
seen highest in age group of 51-60 years 2
(1%) (Fig. 1).

Fig. 1 Age and sex distribution in converted patients


Table III Distribution of difficulty according to
creation of pneumoperitoneum (n=16)
Creation of pneumoperitoneum

Percentage

Previous abdominal surgery

50%

Diffuse peritonitis

6.25%

Cholecystitis

Pancreatitis

Obesity

43.75%

Out
of
70
difficult
cases
pneumoperitoneum creation was found to
be difficult in 16 (22.85%) cases. Maximum

Table IV Distribution of difficulty according to


separation of all adhesion (n=53)
Separation of all adhesion

Percentage

Acute cholecystitis

22

41.50%

Acute pancreatitis

7.54%

Post ERCP cholangitis

12

22.64%

Cirrhotic liver

11.32%

Previous abdominal surgery

16.98%

Out of 70 difficult cases there were 39


(55.71%) cases in which skeletonization,
ligation and division of cystic artery and
duct was difficult. Maximum difficulty in
this step of LC was seen in patients with
abnormal callots anatomy 20 (51.28 %)
(Table V).
Table V Distribution of difficulty according to
skeletonization, ligation and division of cystic artery
and duct (n=39)
Skeletonization, ligation &
division of cystic artery & duct
Short & wide cystic duct
Anomalous vessel
Abnormal Callots triangle
anatomy

Percentage

16

41.02%

7.69%

20

51.28%

There were 16 (22.85%) patients in


which, GB dissection from liver was

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difficult (Table VI). Maximum difficulty


was encountered in this step of LC was due
to Intrahepatic GB 9 (56.25%).

group, we noted maximum conversion rate


in patients having abnormal callots anatomy
7 from 20 patients (35%) (Table IX).

Table VI Difficulty according to excision of GB


from bed (n=16)

Table IX Conversion rate with individual causes

Excision of GB from bed

Conversions

Percentage

Small and contracted GB

43.75%

Intrahepatic GB

56.25%

Different causes
of difficult LC
Acute cholecystitis

Empyema GB

Acute pancreatitis

25%

Post ERCP cholangitis


Abnormal Callots
anatomy
Short and wide cystic
duct
Cirrhotic liver

12

25%

20

35%

16

6.25%

16.66%

Small and contracted GB

28.57%

Out of 70 difficult cases there were 21


(30%) patients in which extraction of GB
from anterior abdominal wall was
difficult. Maximum difficulty in this
particular step of LC was seen in stone
packed gallbladders 8 (38.09%) (Table VII).
Table VII Distribution of difficulty according to
extraction of GB (n=21)
Extraction of GB

Percentage

Large & distended GB

28.57%

Very thick walled rigid GB

33.33%

Multiple calculi

38.09%

Out of 70 difficult LC maximum


conversion to open cholecystectomy rate
was seen in patients with acute cholecystitis
and abnormal Callots anatomy 58.33% each
(Table VIII).
Table VIII Different causes of difficult LC which
had conversion (n=12)

Acute cholecystitis
Acute pancreatitis
Post ERCP
cholangitis
Abnormal Callots
Short and wide
cystic duct
Cirrhotic liver
Small and
contracted GB

n
7

Conversions
Percentage
58.33%

Percentage

22

31.8%

N number of patients from difficult LC group

Mean operating time of 58 difficult


cases which were not converted to open
procedure was 111.4816.96 minutes.
Significant factors which increased the
operating time were; previous abdominal
surgery, intrahepatic gallbladder, multiple
large calculi, very thick walled gallbladder,
anomalous vessels, large and distended
gallbladder (Table X).
Table X Factors association with operating time (n=58)

Previous abdominal surgery

Operating time
(mean SD)
100.45 17.67

P
value
< 0.05

Acute cholecystitis

112.3314.37

> 0.05

Pancreatitis

108.3310.40

> 0.05

11013.78

> 0.05

Post ERCP cholangitis

108.3329.33

> 0.05

Cirrhotic liver

111.217.16

> 0.05

Short and wide cystic duct

107.3310.4

> 0.05

Anomalous vessels

87.8527.66

< 0.05

Abnormal callots

10317.6

> 0.05

120.5524.42

< 0.05

Factors

Obesity

8.33%

25%

58.33%

8.33%

8.33%

Small and contracted GB

10911.4

> 0.05

16.66%

Large and distended GB

97.286.1

< 0.05

Very thick wall GB

12028.50

< 0.05

Multiple Large calculi

104.521.6

< 0.05

Empyema GB

86.2528.39

> 0.05

Studying the conversions from point of


view of individual causes, in difficult LC

Intrahepatic GB

Difficulties in laparoscopic cholecystectomy

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DISCUSSION
Creation of pneumoperitoneum is the
first step of laparoscopic cholecystectomy
and various difficulties can be seen at this
step. In our study after analyzing the
available literature we have found out the
conditions which can make this step of LC
difficult. Out of 200 patients, there were 16
patients who were anticipated to have
difficulty in creating a pneumoperitoneum.
In this maximum anticipation was for the
patients who had previous abdominal
surgeries 8 (50%) and who were obese 7
(43.5%). According to Underwood et al,
intra abdominal adhesions secondary to
previous upper abdominal surgery can tether
underlying viscera consequently increases
the risk of hollow organ injury during
creation of pneumoperitoneum by veress
needle and during placement of laparoscopic
trocars [4]. A prospective study by M.
Hussein et al [5] in obese patients
undergoing laparoscopic cholecystectomy
stated that only technical problem that
necessitated conversion to operation was
failure to establish a pneumoperitoneum.
Once a pneumoperitoneum was established,
each operation followed lines similar to LC
in normal-size patients.
Patients with acute cholecystitis have
oedema,
hypervascularity,
venous
engorgement and gallbladder distension.
Within 72 hours of symptoms the tissue
planes are oedematous and inflamed but are
easier to dissect, having no adhesions at all.
But after 72 hours, the tissue becomes more
friable and becomes dangerous and risky to
dissect. Increased gall bladder wall thickness
is related to the inflammation and fibrosis
that follows attacks of cholecystitis and thus
may reflect difficulty in delineation of the
anatomy during surgery. Problems with
acute biliary pancreatitis are extensive
adhesions, visual road block due to
inflammatory phlegmon in the region of
head of pancreas, highly oedematous cystic
pedicle and hepatoduodenal ligament, and
presence of ascitic fluid. Prior acute
pancreatitis results in scarred and fibrosed
gall bladder and in dense fibrotic adhesions

that renders laparoscopic dissection difficult.


[6,7]
In our study out of 200 patients who
underwent laparoscopic cholecystectomy 22
(11%) patients presented with acute
cholecystitis after 72 hrs of onset of
symptoms. Out of 70 difficult cases, there
were 54 (77.14%) patients who had
difficulty in separating adhesions. Maximum
number of adhesions and difficulty
separating them was seen in patients with
acute cholecystitis 22 (40.74%). Out of 70
difficult cases, there were 4 (7.4%) patients
who had difficulty in separating adhesions
due to pancreatitis.
Out of 70 difficult cases there were 39
(55.71%) cases in which skeletonization,
ligation and division of cystic artery and
duct was difficult. Maximum difficulty in
this step of LC was seen in patients with
abnormal callots anatomy 20 (51.28 %). In
a study conducted by Ajay Anand et al [8]
they found 17.61% patients in their study
group who had wide cystic duct. K. Toress
et al [9] in their study found that 37.6%
patients had an atypical course of cystic
artery. A randomised trial of laparoscopic
versus open cholecystectomy for acute and
gangrenous cholecystitis by Kiviluoto
reported 16% patients in the LC group
requiring conversion and in most cases
because severe inflammation distorting the
anatomy of Callot's triangle [10].
Pawan Lal et al [11] in their study of
73 patients found that 11 patients (15.07%)
with contracted gallbladders, 8 laparoscopic
cholecystectomies were surgically difficult,
and 5 were converted to the open procedure.
Patients with a small contracted gall bladder
or a trabeculated gall bladder due to heavy
stone load and multiple criss cross strictures
in the gall bladder lumen, are also candidates
at risk where the surgeon would have
difficulty in holding the gall bladder [12]. In
our study there were 7 (3.5%) cases that had
small and contracted GB and 9 (4.5%) cases
that had intrahepatic GB, all of these cases
were difficult to operate upon. There were 4
(2%) cases who had empyema GB but were
easy to detach from the liver bed. A gall

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bladder may be congenitally partially or


completely embedded in the liver
parenchyma or may become buried due to
recurrent episodes of inflammation. The
problem relating to this abnormality is an
inability to grasp the fundus of the gall
bladder and an absence of avascular plane of
dissection between the gall bladder and liver
parenchyma, which makes it technically a
challenging task [12]. Malik A et al [13] on
LC in empyema Gall bladder found that the
difficulty level in performing surgery is not
as high as stated in literature if the surgery is
done by experienced surgeons; they
successfully completed LC in 80.59% of
patients with empyema GB.
Thick gall bladder along with large
stones can be difficult to remove, thereby
preventing its excision hence fascial incision
is extended to facilitate its removal [3]. Out
of 70 difficult cases there were 21 (30%)
patients in which extraction of GB from
anterior abdominal wall was difficult.
Maximum difficulty in this particular step of
LC was seen in stone packed gallbladders 8
(38.09%).
Out of 70 difficult LC maximum
conversion to open cholecystectomy was
seen in patients with acute cholecystitis and
abnormal callots anatomy 31.8% each.
Maximum conversion was seen in patients
who presented after 72 hrs of attack of
cholecystitis. There were 7 cases of acute
cholecystitis in which conversion took place.
Out of these 7 cases 4 cases also had
abnormal anatomy at callots, in one patient
there was small and contracted GB in
addition to abnormal callots, 1 patient had
history of post ERCP cholangitis and 1 had
billiary
pancreatitis
associated
with
cholecystitis. The reason for conversion was
dense adhesions around the gallbladder and
in callots triangle which made dissection
extremely
difficult
and
completely
hampering the proceedings.
Significant factors which increased the
operating time were: previous abdominal
surgery, intrahepatic gallbladder, multiple
large calculi, and very thick walled
gallbladder. In all of these cases the P value

was < 0.05. Two other factors which came


out to be significant were anomalous vessels
and large and distended gallbladder. But
these two factors did not increased the
operating time individually. Small sample
size made anomalous vessels significant and
patients having large and distended
gallbladder were not time consuming to
extract them from the abdominal wall. But
two factors acute cholecystitis and abnormal
callots anatomy are above all of them and
did not come out to be significant. The
reason can be explained as maximum
numbers of cases were converted to open
cholecystectomy
because
of
acute
cholecystitis and abnormal callots anatomy
and the mean operating time was also high
in both the groups which were almost equal
to the mean operating time of the difficult
cases.
CONCLUSION
We conclude that previous abdominal
surgery, intrahepatic gallbladder, multiple
large calculi, very thick walled gallbladder,
acute cholecystitis and abnormal Callots
anatomy are the difficult factors to operate
upon and increases the operating time. Acute
cholecystitis and abnormal callots anatomy
are the two conditions in which the
conversion rate is higher.
CONFLICT OF INTERESTS
Authors have no conflict of interests to
declare.
REFERENCES
1. Hunter
JG,
Trus
T.
Laparoscopic
cholecystectomy. In: Nyhus LM, Baker RJ,
Fisher JE editors. Mastery of surgery. 3rd ed.
Boston: Little brown and company; 1997.
p. 1098.
2. Capizzi FD, Brulati FM, Boschi S, et al.
Conversion rate in laparoscopic cholecystectomy
evaluation from 1993 and current state. Journal
of Laparoscopic and Advanced Surgical
Technique. 2003; 13(2): 7-13.
3. Palanivelu
C.
Difficult
Laparoscopic
Cholecystectomy. In: Parthasarathi R, editor.
Art of Laparoscopic Surgery. Textbook and
Atlas. 1st ed. India: Jaya Publications; 2005. p.
607-634.

Difficulties in laparoscopic cholecystectomy

155
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4. Underwood RA, Soper NJ. Laparoscopic


cholecystectomy and choledocholithotomy. In:
Blumgart LH, Fong Y editors. Surgery of liver
and biliary tract. 3rd ed. London: W.B.
Saunders Company Ltd; 2002. p. 709-712.
5. Hussien M, Appadurai IR, Delicata RJ.
Laparoscopic cholecystectomy in the grossly
obese: 4 years experience and review of
literature. HPB Oxford. 2002; 4(4): 157-161.
6. Rattner DW, Ferguson C, Warshal AL. Factors
associated with successful laparoscopic
cholecystectomy for acute cholecystitis. Ann
Surg. 1993; 217(3): 233-236.
7. Nachani J, Supe A. Pre operative prediction of
difficult laparoscopic cholecystectomy using
clinical and ultrasonographic parameters.
Indian J Gastroenterol. 2005; 24: 16-18.
8. Anand A, Pathania BS, Singh G. Conversion in
laparoscopic cholecystectomy: an evaluation
study J Med Educ. 2007; 9: 171-174.

9. Torres KA, Golonka CA. The course of the


cystic
artery
during
laparoscopic
cholecystectomy. Folia Morphol. 2005; 68(3):
140-143.
10. Kiviluoto T, Sinen J, Lwkkanen P.
Randomized trial of laparoscopic versus open
cholecystectomy for acute and gangrenous
cholecystitis. The Lancet. 1998; 351: 321-325.
11. Lal P, Agarwal PN, Malik VK. A difficult
laparoscopic cholecystectomy that requires
conversion to open procedure can be predicted
by preoperative USG. JSLS. 2002; 6(1): 59-63.
12. Khanna S. How to predict difficult
laparoscopic cholecystectomy and when to
convert.
[available
online
at
http://www.iages.org.in/media/files/chapter10.
pdf. Aug 10 2011]
13. Malik A, Laghari AA, Altaf K, et al.
Laparoscopic cholecystectomy in empyema of
gall bladder: An experience at Liaquat
University Hospital, Jamshoro, Pakistan. J
Minim Access Surg. 2007; 3(2): 52-56.

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Sahu SK. et al.

ORIGINAL ARTICLE

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IS GASTROESOPHAGEAL REFLUX DISEASE INFLUENCED


BY DUODENOGASTRIC REFLUX ?
Mihaela-Aura Mocanu1 , M. Diculescu1, T. Nicolae1, Monica Dumitrescu2
1) Gastroenterology, Endoscopy and Hepatology Elias Clinic, Bucharest, Romania

2) Department of Statistics, University of Bucharest, Romania


IS GASTROESOPHAGEAL REFLUX DISEASE INFLUENCED BY DUODENOGASTRIC
REFLUX ? (Abstract): BACKGROUND: It is well known that the gastroesophageal reflux is a
frequent disease in medical practice. A lot of factors are involved in its pathogenesis. The aim of
our study was to find out if the duodenogastric reflux is one of these factors. We also looked for
the pathological conditions associated with duodenogastric reflux. MATERIAL AND
METHODS: We studied a lot of 59 cases (30 females and 29 males) with ages between 39 and 54
years old suffering from gastroesophageal reflux disease (GERD). GERD, duodenogastric reflux
were confirmed by upper gastrointestinal endoscopy. The abdominal ultrasound exam were used
to evaluate the duodenal and gallbladder motility (ejection fraction, EF). The severity of GERD
was appreciated using GERD Q-score. RESULTS: The women to men ratio was 30 to 29 and the
mean age was 42 2 years. Cholesterolosis was found in 45.7% (n=27) from the patients. From
these patients, 92.6% (n=25) had a ejection fraction (EF) above normal (hyperkinesia) and only
two patients had normal gallbladder motility. From the patients with cholesterolosis, 20 (74%)
had duodenogastric reflux. The other 32 patients without cholesterolosis had no duodenogastric
reflux neither. We noted a strong statistical correlation between the cholesterolosis and
duodenogastric reflux (P=1,115x10-8). The duodenogastric reflux was found in 33.89% (n=20)
from the patients and half of them (n=10) had associated esophagitis; we found a strong statistical
correlation between duodenogastric reflux and esophagitis: P=1,543x10-13. All the patients had
GERD Q-scores higher than 7 points; the mean score was 11.254.04 points (range 8-18). The
mean Q-score value for the cases with duodenogastric reflux was 16.23.37; the cases without
duodenogastric reflux (n=39) had a mean Q-score of 9.21.23 (P=3,138x10-9). CONCLUSION:
These results suggest that biliary disease can contribute to the duodenogastric reflux and the
duodenogastric reflux aggravates gastroesophageal reflux.
KEY WORDS: GASTROESOPHAGEAL REFLUX; DUODENOGASTRIC REFLUX;
DUODENAL MOTILITY; GALLBLADDER MOTILITY; GALLBLADDER EJECTION
FRACTION; GERD Q SCORE
SHORT TITLE: Gastrooesophageal & duodenogastric reflux
HOW TO CITE: Mocanu MA
M, Nicolae T., Dumitrescu M. Is gastroesophageal reflux disease influenced by
duodenogastric reflux ? Jurnalul de chirurgie (Iai). 2013; 9(2): 157-160. DOI: 10.7438/1584-9341-9-2-6.

INTRODUCTION
Our interest for gastroesophageal
reflux is due to the high frequency of this
disease. The well-known causes of
gastroesophageal reflux disease (GERD) are:
impaired esophageal clearance, the altered
antireflux mechanism and the diminished
gastric motility. The antireflux mechanism
include: the pressure of low esophageal

sphincter, Hisss angle and the abdominal


part of esophagus. There are some date
which describe also a duodenogastric reflux
associated with gastric ulcer, esophagitis and
gallbladder lithiasis [1,2].
We wanted to know how frequent the
duodenogastric reflux in patients with
GERD is. We also tried to find which are
associated disease with the duodenogastric

Received date: 20.01.2013


Accepted date: 16.03.2013
Correspondence to: Dr. Mihaela-Aura Mocanu,
Gastroenterology, Endoscopy and Hepatology, Elias Clinic, Bucharest, Romania
Bd. Mrti No 17, Sector 1, 011461, Bucharest, Romania
Phone: 0040 (0) 21 316 16 00
Fax: 0040 (0) 21 316 16 02
E-mail: mmocanu2005@gmail.com

158

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reflux and if the duodenogastric reflux can


aggravate GERD.
MATERIAL AND METHODS
We retrospectively reviewed 59
patients with GERD. Different data
(demographic, GERD severity, duodenogastric reflux, gallbladder ejection fraction,
duodenal motility) were analysed.
The diagnosis of GERD was done
using clinical data and upper endoscopy
examination. The duodenogastric reflux was
also proved by upper digestive endoscopy
(bile inside the stomach).
The abdominal ultrasound examination
was used to diagnose the gallbladder
diseases and to evaluate the gallbladder
motility; in this way we calculated
gallbladder volume (V) using the formula
V = 0.5 x L x l x g where L is the gallbladder
length, l is the width of gallbladder and g is
the thickness of gallbladder wall [3]. The
ejection fraction (EF) was then calculated
using the formula EF = V1-V2 / V1 x 100

were V1 is the fasting gallbladder volume


and V2 is the volume after the ingestion of
Boyden meal. Normal EF values are 50 to
60%; the cases with higher values were
noted as hyperkinesia. The duodenal
motility was also evaluated using abdominal
ultrasound exam and it was noted as
normal or increased.
In order to evaluate the GERD we
calculated the GERD Q-score [4-6]. The Qscore contains 6 questions: 4 items about
symptoms and 2 items about the impact of
symptoms on the patients life (health related
quality of life) (Table I). The answers are
filled in by the patient and than evaluated by
the doctor. The total score was calculated by
adding the point values for each
corresponding answer. Increasing scores
correlated with GERD severity (Table I).
Data were included in a MS Excel
database and statistically analyzed; bivariate
analysis (t test and 2 test) was used. A
P < 0.05 was considered statistically
significant.

Table I GERD Q score questionnaire [4]


Symptoms and health related quality of life (HQLR)
How often have you had burning sensation in the chest
(heatburn) ?
How often have you felt food or liqiud stomach contents
turning it in the mouth or throat (regurgitation) ?
How often have you had pain in the upper abdomenum
(epigastric pain) ?
How often have you had nausea ?
How often have you had trouble sleeping due to
heartburn or regurgitation ? (HQLR - item)
How often have you taken medication for heartburn and
regurgitation further other than those prescribed by a
doctor (ranitidine, maalox, dicarbocalm) (HQLR - item)

How many times does this occur per week?


0 Days

1 Day

2 to 3 Days

4 to 7 Days

0p

1p

2p

3p

0p

1p

2p

3p

3p

2p

1p

0p

3p

2p

1p

0p

0p

1p

2p

3p

0p

1p

2p

3p

The total score is interpretated as follows: 0 to 2: no probability of GERD; 3 to 7: Low probability of GERD (50% likelihood of GERD);
8 to 10: GERD (discomfort disturbing symptoms); 11 to 18: severe GERD (discomfort disturbing symptoms)

RESULTS
The women to men ratio was 30 to
29 and the mean age was 42 2 years.
Cholesterolosis was found in 45.7%
(n=27) from the patients; 54.3% (n=32) did
not have any gallbladder diseases. From the
patients with cholesterolosis, 92.6% (n=25)
had a ejection fraction (EF) above normal

(hyperkinesia) and only two patients had


normal gallbladder motility (EF 50 to 60%).
From the patients with cholesterolosis,
twenty (74%), had duodenogastric reflux.
The other 32 patients without cholesterolosis
had no duodeno-gastric reflux neither.
We noted a strong statistical
correlation between the cholesterolosis and

Gastrooesophageal & duodenogastric reflux

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Jurnalul de Chirurgie (Iai), 2013, Vol. 9, Nr. 2

duodenogastric
reflux
(2
test;
-8
P = 1,115 x 10 ).
The duodenogastric reflux was found
in 33.89% (n=20) from all the patients and
half of them (n=10) had associated
esophagitis; we found a strong statistical
correlation between duodenogastric reflux
and esophagitis: 2 test; P = 1,543 x 10-13.
All the patients with duodenogastric
reflux (100%; n=20) had increased duodenal
motility too. Among the other 39 patients
without duodenogastric reflux, only 12.8%
(n=5) had increased duodenal motility; this
correlation is also statistically significant (2
test; P = 8,439 x 10-10). We noted similar
results for galbladder hyperkinesia: all the
patients with duodenogastric reflux (100%;
n=20) versus five patients (12.8%)
without duodenogastric reflux (2 test;
P = 8,439 x 10-10).
All the patients from the study group
had GERD Q-scores higher than 7 points;
the mean score was 11.254.04 points
(range 8-18). 67.8% (n=40) had a Q-score of
8 to 10 (mean: 91.13; range: 8-10) and
32.2% (n=19) had a score of 11 to 18 (mean:
163.27; range: 11-18).
The mean Q-score value for the cases
with duodenogastric reflux was 16.23.37;
range: 8-18; out of 20 cases with
duodenogastric reflux, 35% (n=7) had high
GERD Q-scores (11 to 18) and associate
esophagitis demonstrated by endoscopy. The
cases without duodenogastric reflux (n=39)
had a mean Q-score of 9.21.23 (range 818): The Q-score was statistically higher in
duodenogastric reflux group (t test;
P = 3,138 x 10-9).
We also noted significant higher Qscores values for the patients with
gallbladder hyperkinesia (14.164.06 vs
91.26; t test; P = 1,688 x 10-9) and for the
patients with increased duodenal motility
(14.54.38 vs 9.21.02; t test; P=2,832 x 10-8).
DISCUSSION
The duodenogastric reflux was
described in about 25% cases of patients
with GERD according to the paper of
Brillantino A et al. [1]. They described

duodenogastric reflux associated with gastric


ulcer, gallbladder lithiasis and esophagitis
and they pointed that the duodenogastric
reflux can damage the gastric and
esophageal mucosa due to the fact that it
contains biliary acids and pancreatic juice
[7-8]. It is not clear if the duodenogastric
reflux can sometimes be found with normal
people as a physiological event or is a
pathological dismotily associated with
gastroesophageal reflux.
In our paper, we noticed that
duodenogastric reflux is found in 34% of
patients with GERD versus 25% mentioned
in Brillantinos paper [1].
The duodenogastric reflux differs from
transpiloric flow in the fact that it operates
the bile and pancreatic juice inside the
stomach and it happens in the interdigestive
phase. Johnson AG noticed that none of
these waves of transpiloric retrograde flow is
due to antiperistalsis waves from D2 [9].
In experimental study done on
volunteers by intubation technique Keane
FB et al. [8] have been measured the antral
and duodenal pressure, the pH, the levels of
bicarbonate, biliary acids and trypsin in
gastric
and
duodenal
juice.
The
polientilenglicol (PEG) was used as a
marker which indicates the direction of fluid
movement. All the data were recorded
simultaneously with the phases of
interdigestive motor complexes (IMC).
The
authors
found
that
the
duodenogastric reflux has two components:
the secretory phases which occur before
phase III of IMC and the motor phase which
occurs in the II phase of IMC. Due to the
fact that after the phase III of IMC the
contents of duodenogastric reflux is
evacuated from the stomach we can say that
III phase acts as a gastric clearance.
In our study we found that all cases of
gallbladder cholesterolosis have high values
of EF meaning hyperkinesia. We also
noticed that cholesterolosis is associated
with enhanced duodenal motility.
These facts allow us to speculate that
the gallbladder bile which contains a large
amount of cholesterol and which is

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Jurnalul de Chirurgie (Iai), 2013, Vol. 9, Nr. 2

evacuated quickly in the duodenum can


induce an enhanced duodenal motility.
The duodegastric reflux requires two
conditions: the pylorus opening and the
retrograde duodenal motor wave. We think
that enhanced duodenal motility can fulfill
these two conditions. So, the gallbladder
cholesterolosis can be one of the etiological
factors which produce duodenogastric
reflux.We did not exclude a lot of other
patological conditions wich can produce
duodenogastric reflux alsa well as a methods
for its diagnosise [10-16].
All cases with duodenogastric reflux
have high GERDQ score that means the
duodenogastric reflux can aggravate
gastroesophageal reflux; in this way, from
the 20 cases with duodenogastric reflux, 10
cases had esophagitis.
CONCLUSIONS
The
duodenogastric
reflux
is
associated with GERD in 34% from cases.
The association of duodenogastric reflux
with gallbladder cholesterolosis can induce
the supposition that duodenal bile rich in
cholesterol can be the trigger for enhanced
duodenal motility and duodenogastric reflux
which may aggravate gastroesophageal
reflux.
CONFLICT OF INTERESTS
Authors have no conflict of interests to
declare.
AKNOWLEDGEMENTS
The corresponding author is PhD
student of University of Medicine and
Pharmacy Carol Davila Bucureti. This
paper is the result of the research activity
during the doctoral internship.

REFERENCES
1. Brillantino A, Monaco L ,Schettino M, et al.
Prevalence of pathological duodenogastric
reflux and the relationship between
duodenogastric and duodenogastroesophageal
reflux in chronic gastroesophageal reflux
disease. Eur J Gastroenterol Hepatol. 2008;
20(12): 1136-1143.

2. Thompson DG. Duodenogastric reflux is there


any progress Br Med J. 1982; 284: 845-846.
3. Sporea I, Gluhovschi G. Ghid practic de
ecografie abdominal. Timioara: Editura
Helicon; 1999. p. 152-167.
4. Ebell MH. Diagnosis of gastroesophageal
reflux disease. Am Fam Physician. 2010;
81(10): 1278-1280.
5. Halling K. Development of an enhanced
questionnaire
for
the
diagnosis
of
gastroesofageal reflux disease based on the
Reflux Disease Questionnaire, the GERD
Impact Scale and the Gastrointestinal
Symptom Rating Scale. Gut. 2007; 56(Suppl
III): A 209.
6. Mocanu M, Diculescu M, Nicolae T.
Evaluarea particularitilor bolii de reflux la
pacienii cu hernie gastric transhiatal i
steatoz hepatic din perspectiva eficientizrii
acestei asocieri. Teza doctorat. U.M.F.
Bucureti; 2013.
7. Heading RC. Duodenogastric reflux. Gut
1983; 24: 510-518
8. Keane FB, Dimango EP, Malagelada JR.
Duodenogastric reflux in humans: its
relationship to fasting antroduodenal motility
and gastric pancreatic and biliary secretion
gastroenterology. Gastroenterol. 1981; 81:
726-731.
9. Jonson AG. Peptic ulcer and the pilor. Lancet.
1979; 1: 710-712.
10. King A, Macdonald C, Orn C. Understanding
gastroesophageal reflux disease(GERD): a
patient segmentation analysis. Scand J
Gastroenterol. 2007; 42(Suppl 244): 21.
11. Orban-chiopu A, Mocanu M. Litiaza
vezicular asociat steatozei hepatice non
alcoolice. Journal of Gastrointestinal and
Liver Disease. 2007; 16 (suppl 1): 16
12. Mosteanu O, Pop Acalovshi M. Motilitatea
veziculei biliare la pacienii cu steatohepatita
nonalcooloca-evaluare ecografic. Journal of
Gastrointestinal and Liver Disease. 2007;
16(suppl. 1): 16-17.
13. King MP, Adam RD, Pryde A, Mc Dicken
WN, Heading RC. Relationships of human
antroduodenal motility and transpyloric fluid
movement noninvasive observations worth
real-time ultrasound Gut. 1984; 25: 13841391.
14. Tack J, Bisschops R, Koek G. Dietary
restrictions during ambulatory monitoring of
duodenogastroesophageal reflux. Dig Dis Sci.
2003; 48(7): 1213-1220.
15. .Fein M, Fuchs KH, Bohrer T, et al. Fiberoptic
technique for 24 hour bile reflux monitoring
standards and normal values for gastric
monitoring. Dig Dis Sci. 1996; 41(1): 216-225.
16. Lazarescu A, Sifrim D. Ambulatory
monitoring of GERD current technology
Gastroenterol Clin North Am. 2008; 37(4):
793-805.

ARTICOLE ORIGINALE

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COMPLICAIILE PRECOCE ALE CHIRURGIEI


CATARACTEI
C. Constantin, I. Cijevschi, Silvia Slceanu, C. David
Clinica de Oftalmologie, Spitalul Clinic Universitar Ci Ferate Iai
EARLY COMPLICATIONS OF CATARACT SURGERY (Abstract): BACKGROUND: There
are different complications of the cataract surgery described in the literature. The impact of these
complications on the visual function is in correlation with many factors, some of them being
imprecise and unable to be used as prognostic factors before and after the surgery. The modern
technique and the surgeons experience lowers the complications incidence to a minimum, but
even so, some problems cannot be avoided. AIM: The aim of this study is to analyse the early
cataract surgery complications for patients operated in 2012 at the Ophthalmology Unit, Railway
Hospital, Iai. MATERIAL AND METHOD: We conducted a retrospective analysis of the
medical records of the patients who underwent cataract surgery in 2012. There were a total of 480
cataract surgeries, the majority of them (92,7%) being age related cataracts in different stages of
evolution, of which 31.45% being mature cataracts. In 476 eyes, artificial lens was inserted perprimam (474 eyes with posterior chamber intraocular lens and 2 eyes with anterior chamber
intraocular lens), in one case the posterior chamber intraocular lens was sutured to the sclera, in 3
cases the eyes remained without lens. RESULTS: The incidence of severe complications or with
potential of severe development was: severe corneal oedema 0.83% (4 cases), remaining lens
fragments in the vitreous cavity 0.62% (3 cases), toxic anterior segment syndrome (TASS) 0.41%
(2 cases). There were no endophthalmitis, expulsive haemorhage or retinal detachment after
cataract surgery. CONCLUSIONS: The number of early complications of our patients is the same
with numbers shown in other studies. With a better surgical technique, a good examination of the
patient, a thorough explanation of the procedure to the patient, the use of high quality substances
during surgery and proper technology we can lower even more the incidence of the complications.
KEY WORDS: CATARACT; SURGERY; PHACOEMULSIFICATION; EXTRACAPSULAR
CATARACT EXTRACTION
SHORT TITLE: Complicaiile chirurgiei cataractei
Complications of cataract surgery
HOW TO CITE:
. [Early complications of cataract surgery]. Jurnalul de
chirurgie (Iai). 2013; 9(2): 161-165. DOI: 10.7438/1584-9341-9-2-7.

INTRODUCERE
Chirurgia modern a cataractei
permite, pe de o parte, datorit progresului
tehnic, o recuperare rapid a funciei vizuale
n post-operatorul imediat i pe de alt parte
o reducere important a frecvenei
incidentelor i complicaiilor intra- i postoperatorii. Cu toate acestea, n crile de
specialitate sunt menionate suficient de
multe complicaii ale chirurgiei cataractei
dintre care unele cu potenial major de
impact negativ asupra rezultatului final.

Lucrarea i propune s analizeze


incidena complicaiilor dup chirurgia
cataractei aprute la pacienii operai n
Clinica Oftalmologic a Spitalului Ci
Ferate Iai n perioada 1.01.201231.12.2012, analiznd factori de risc pre i
postoperatori
cu
impact
asupra
complicaiilor postoperatorii.
MATERIAL I METOD
Am analizat retrospectiv foile de
observaie ale pacienilor operai de cataract

Received date: 15.01.2013


Accepted date: 20.02.2013
Adresa de coresponden: Dr. Ctlin Constantin
Clinica de Oftalmologie, Spitalul Clinic Universitar Ci Ferate Iai
Str. Garabet Ibrileanu, nr. 1, 700506, Iai, Romania
Tel.: 0040 (0) 232 21 64 22
E-mail: catalin.p.constantin@gmail.com

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n perioada 01.01.2012-31.12.2012. Pacienii


luai n studiu au efectuat un examen
oftalmologic complet (examinare pol
anterior, pol posterior acolo unde stadiul
de evoluie al cataractei a permis acest lucru
, acuitate vizual, presiune intraocular). Sau realizat pentru fiecare pacient evalurile
biometrice oculare specifice n vederea
calculrii puterii dioptrice a cristalinului
artificial ce urma a fi implantat. De
asemenea, s-a efectuat pentru fiecare pacient
un examen general de medicin intern
pentru precizarea strii generale de sntate
n vederea evalurii riscului anestezic.
Au fost analizate datele din registrul de
protocol operator privind incidentele intraoperatorii survenite n cursul interveniei
chirurgicale i complicaiile postoperatorii
(consemnate n foile de observaie).
Interveniile chirurgicale au fost
efectuate de doi medici care au utilizat dou
tehnici chirurgicale de operare a cataractei
(facoemulsificare i respectiv extracia
extracapsular manual - EEM) cu
urmtoarele
variante
tehnice:
facoemulsificare prin incizie scleral 2,75
mm
tehnica
tilt
and
tumble,
facoemulsificare prin incizie limbic
anterioar 2,2 mm tehnica chop sau stop
and chop, extracie extracapsular prin
incizie scleral tunelizat de 6 mm.
Asepsia zonei operatorii a fost
asigurat prin toaleta local cu betadin, iar
anestezia a fost n majoritatea cazurilor
local (peribulbar sau retrobulbar),
existnd i cteva situaii n care s-a operat
sub
anestezie
general.
Profilaxia
endoftalmitei s-a fcut prin injecie
subconjunctival sau peribulbar cu
gentamicin i dexametazon, mai rar cu
Cefuroxim intra-cameral.
REZULTATE
n
perioada
luat
n
studiu,
01.01.2012-31.12.2012, s-au efectuat 480
intervenii pentru cataract, la un numr de
451 pacieni, 247 femei i 204 brbai.
Pacienii au avut vrste cuprinse ntre
11 ani i 91 ani, media de vrst fiind
71,59,9 ani.

Analiza grupelor de vrst a artt o


distribuie gaussian cu un maxim pentru
decada 70-79 ani (Fig. 1).

Fig. 1 Distribuia pe grupe de vrst

Tipurile de cataract operat au fost: n


4 cazuri cataract hipermatur (0,83%), 140
cazuri cataract matur (29,16%), n 305
cazuri cataract n evoluie (63,54%), n 18
cazuri cataract presenil n evoluie
(3,75%), n 7 cazuri cataract presenil
matur (1,46%), 3 cazuri cu cataract
traumatic (0,63%), 2 cazuri de cataract
congenital (0,41%), 1 caz cataract
complicat post-uveitic (0,2%).
Am notat n 23 cazuri prezena
sindromului pseudoexfoliativ cu sau fr
glaucom secundar (4,79%).
Au fost efectuate un numr de 381 de
intervenii prin facoemulsificare (79,37%),
98 intervenii de EEC manual (20,41%), o
extracie intracapsular (0,2%); au fost
implantate n 474 de cazuri cristaline
artificiale de camer posterioar (98,75%),
n 2 cazuri cristaline de camer anterioar
(0,41%), un caz de cristalin cu sutur la
scler (0,2%) i 3 cazuri (0,62%) au rmas
cu afakie post-operatorie.
n ceea ce privete pacienii afaci au
existat dou situaii de implantare per
secundam de pseudofak de camer
posterioar pe suportul capsular restant (in
sulcus).
Durata medie de spitalizare a
pacienilor operai de cataract a fost de
6,842,55 zile, cu un interval pre-operator
mediu de 3,382,18 zile i un interval mediu
post-operator de 2,461,36 zile.

Complicaiile chirurgiei cataractei

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Complicaiile postoperatorii cele mai


frecvente au fost edemul corneean i
congestia conjunctival (Tabelul I).
Tabel I Incidena
postoperatorii

complicaiilor

Complicaia
n
Complicaii precoce minore
Edem cornean minor
136
Congestie conjunctival moderat
112
Edem cornean moderat
74
PIO crescut
10
Cute descemetice
9
Vitrectomie anterioar
5
Hemoragie subconjunctival
3
Material cristalinian n CV
3
Afakie post-operatorie
3
Pupil deformat
2
Colobom irian iatrogen
1
Compliaii precoce majore
Edem cornean sever*
4
Complicaii tardive minore
Reintervenie**
1
Complicaii tardive majore
Edem cornean sever*
4
TASS
2

28,33
23,33
15,42
2,08
1,87
1,04
0,62
0,62
0,62
0,42
0,21

deosebite. Nu am ntlnit cazuri cu ametropii


extreme sau globi vitrectomizai.
Anumite dificulti tehnice n cursul
operaiei (utilizarea ultrasunetelor n exces,
instabilitatea camerei
anterioare sau
profunzimea ei redus, inciziile imperfecte,
etc.) au o legtur direct cu o serie de
complicaii precoce ale chirurgiei cataractei,
dar acestea nu reprezint totui o regul
ntotdeauna valabil [5,6]. Dar multe din
incidentele intra-operatorii cu impact asupra
evoluiei post-operatorii ct i multe dintre
complicaiile post-operatorii nu au un
determinism direct legat de o cauz
specific, apariia lor fiind oarecum
ntmpltoare. n ceea ce ne privete, pentru
complicaiile severe pe care le-am raportat
(edem cornean sever, TASS) nu am reuit s
stabilim un determinism direct concret.

0,83

Tabel II Rata complicaiilor chirurgiei cataractei


(dup BCSC ediia 2010-2011) [7]

intra-

Complicaia

incidena

0,21

Major, precoce
Endoftalmita

0,83
0,42

PIO presiune intraocular; CV cavitatea vitrean; TASS Toxic


Anterior Segment Syndrome; * aceleai cazuri; ** reintervenie
pentru resturi corticale

DISCUII
Complicaiile chirurgiei cataractei au
suferit o serie de schimbri de-a lungul
timpului att ca tipologie ct i ca inciden
odat cu evoluia tehnicilor chirurgicale.
Chirurgia modern, care se desfoar
oarecum pe un glob ocular nchis permite o
recuperare rapid a funciei vizuale n
condiiile unei securiti crescute n timpul
momentului operator. O serie de condiii
speciale ale globului ocular cresc incidena
complicaiilor intra- i post-operatorii
(sindromul pseudoexfoliativ [1], globul
ocular subdimensionat sau supradimensionat
ametropiile extreme [2], subluxaiile de
cristalin [3], globii vitrectomizai [4] etc.).
n cazuistica noastr am avut un
procent de 4,79% cataracte cu sindrom
pseudoexfoliativ, cu sau fr glaucom
asociat, dar care nu au determinat situaii

mediana

0-1,9%

0,13%

0-6%

0,3%

0-7,8%

1,1%

0-7,6%

1,4%

0-2%

0,7%

Major, tardiv
Keratopatie buloas
Dislocarea pseudofak
Edem macular cistoid
semnificativ clinic
Decolare de retin

Alte complicaii precoce


Plag dehiscent /
0-3%
prolaps irian
Hemoragie n camera
0-4%
anterioar
Hypopion
0-2%
Traumatism irian
Ruptur zonular/capsular
posterioar
Pierdere de vitros

0,6%
0,5%
0,2%

0-9,1%

1,3%

0-9,9%

3,1%

0-4%

0,8%

Hemoragie vitreean

0-8%

0,3%

Hemoragie coroidian

0-2%

0,3%

Alte complicaii tardive


Uveita
Presiune intraocular
crescut (cu unghi nchis)
Presiune intraocular
crescut (cu unghi deschis)
Opacifierea capsulei
posterioare

0-13,3%

1,8%

0-1,6%

0,2%

0-19,6%

1,2%

0,7-47,6%

19,7%

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Complicaiile chirurgiei cataractei pot


fi clasificate dup mai multe criterii. Am
ales o clasificare bazat pe o sintez a
literaturii de specialitate preluat din BCSC
ediia 2010-2011 (Tabelul II) [7].
Acestea sunt doar o parte a
complicaiilor chirurgiei cataractei. Mai sunt
menionate, n diverse alte lucrri ca i
complicaii precoce: camera anterioar de
profunzime mic, material cristalinian
restant n camera posterioar/camera
anterioar, astigmatismul indus chirurgical,
sindromul toxic de segment anterior,
sindromul
Brown-McClean, sindromul
uveit-glaucom-hifem, decolarea/rupturile
membranei Descemet, keratoliza, surprizele
refractive, iar ca i complicaii tardive:
invazia
epitelial
a
camerei
anterioare, fimoza capsulei anterioare,
alterarea zonular tardiv cu dislocarea
pseudofakului [8].
Desigur c impactul asupra recuperrii
funciei vizuale i a rezultatului postoperator final difer de la complicaie la
complicaie, unele avnd un impact minor,
chiar dac persist un timp mai ndelungat,
altele alternd ireversibil funcia vizual i
determinnd un prognostic infaust chiar din
perioada post-operatorie imediat.
Situaia este uneori dificil de estimat
pentru unele complicaii, pentru c n ciuda
unui aceluiai tip de manifestare clinic
evoluia i prognosticul pot fi extrem de
diferite. De exemplu, edemul cornean postoperator, care are etiologie multifactorial
extrem de divers, poate n aceleai condiii
s constituie o complicaie major sau
dimpotriv, s fie un fenomen pasager cu
evoluie favorabil fr ca vreun element
clinic ajuttor s fie definitoriu n aprecierea
prognosticului.
n studiul nostru, complicaiile
consemnate au fost n mare parte minore
(Tabelul I). Au existat situaii n care
cazurile care au necesitat vitrectomie
anterioar (din cauza rupturilor capsulare cu
sau fr material cristalinian n cavitatea
vitrean) au avut ulterior un parcurs
favorabil; dou cazuri au dezvoltat ns
edem macular cistoid semnificativ clinic

(fiind complicaii tardive nu sunt


consemnate n studiu).
Au existat i dou situaii de sindrom
toxic de segment anterior (TASS)
consemnate ca atare de la nceput, dei
numrul de edeme corneene severe a fost
mai mare dar, ntr-un parcurs de urmrire
mai lung, s-au remis n intervale de timp
variabile. Nu am nregistrat alte complicaii
severe, de tipul hemoragiei expulzive,
hemoragiei vitreene, decolrii de retin,
endoftalmitei post-operatorii.
Din totalul de 480 ochi operai pentru
cataract 28% au prezentat un edem cornean
minor care s-a remis n cteva zile cu sau
fr tratament local.
Cauzele sunt multiple, de la duritate
crescut a nucleului ce a necesitat o cantitate
mare de ultrasunete, pn la profunzimea
redus a camerei anterioare care face ca
manevrele chirurgicale, n special eliberarea
de ultrasunete, s se fac n vecintatea
endoteliului cornean, numrul de celule
endoteliale, timpul de phacoemulsificare,
substanele vscoelastice folosite, experiena
chirurgului i aparatul folosit pentru
intervenie. Edemul cornean moderat s-a
ntlnit n 15,14% din cazuri, iar cel sever n
0,83% cazuri n care credem c o contribuie
major la instalarea edemului l-a avut
numrul sczut de celule endoteliale.
n literatur sunt menionate situaii de
edem cornean sever care nu se datoreaz
numrului mic de celule endoteliate cum
este cazul n TASS, incidena acestuia fiind
ntre 1,87% i sub 1% [9,10].
Celelalte complicaii imediate ntlnite
sunt n procent de sub 1 %, au fost rezolvate
n postoperatorul imediat sau tardiv,
necontabiliznd nici un caz de pierdere a
vederii. Ochii iniial afaci au fost implantai
ulterior cu implant de camer posterioar n
sulcus. Edemele corneene au beneficiat de
tratatment
prelungit
cu
colire
cu
dexametazon
i
soluii
hipertone
administrate topic.
Considerm c experiena chirurgului
este importnat n reducerea incidenei
complicaiilor
intra-operatorii.
Studiul
efectuat n doua centre din Japonia cu medici

Complicaiile chirurgiei cataractei

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Jurnalul de Chirurgie (Iai), 2013, Vol. 9, Nr. 2

rezideni atest mbuntirea performanei


individuale n timp [11].
CONCLUZII
Complicaiile imediate ale chirurgiei
cataractei au un impact semnificativ, n
special asupra chirurgului, acesta ncercnd
n mod firesc s le elimine sau mcar s le
scad incidena. Orice operaie expune
pacientul la riscuri, dar pregtirea
preoperatorie de calitate, diagnosticul exact,
evaluarea cazului, mbuntirea continu a
tehnicii chirurgicale, i nu n ultimul rnd
suportul tehnologic i experiena chirurgului
fac ca aceste riscuri s fie minime.
Rata complicaiilor postoperatorii
imediate ntlnite n cazuistica noastr
coincide cu datele din literatura de
specialitate.
CONFLICT DE INTERESE
Autorii nu declar nici un conflict de
interese.
BIBLIOGRAFIE
1. Sufi AR, Singh T, Mufti AA, Rather MH.
Outcome of phacoemulsification in patients
with and without pseudoexfoliation syndrome
in Kashmir. BMC Ophthalmol. 2012; 12: 13.
doi: 10.1186/1471-2415-12-13.
2. Fesharaki H, Peyman A, Rowshandel M, et al.
A comparative study of complications of
cataract surgery with phacoemulsification in
eyes with high and normal axial length. Adv
Biomed Res. 2012; 1: 67. doi: 10.4103/22779175.102971.

3. Goel R, Kamal S, Kumar S, et al. Feasibility


and
complications
between
phacoemulsification and manual small incision
surgery
in
subluxated
cataract.
J Ophthalmol. 2012; 2012: 205139. doi:
10.1155/2012/205139.
4. Raizada S. Phacoemulsification and pars plana
vitrectomy: a combined procedure (comment)
Indian J Ophthalmol. 2007; 55(6): 487-488.
5. Jaffe NS, Jaffe MS, Jaffe GF. Catarct Surgery
and Its complications. 6th ed. St. Louis:
Mosby; 1997.
6. Powe NR, Schein OD, Gieser SC, et al.
Synthesis of the literature on visual acuity and
complications following catarct extraction
with intraocular lens implantation. Arch
Ophthalmol. 1994; 112(2): 239-252.
7. Bobrow JC, Blecher MH, Glasser D, et al.
Basic and Clinical Science Course, Section 11:
Lens and cataract. 2010-2011. American
Academy
of
Ophthalmology;
ISBN
9781615251391.
8. Steinert RF. Cataract Surgery: Technique,
Complications, and Management. 2nd ed.
Philadelphia: Saunders; 2004. p. 507-513.
9. Choi JS, Shyn KH. Development of toxic
anterior segment syndrome immediately after
uneventful phaco surgery. Korean J
Ophthalmol. 2008; 22(4): 220-227. doi:
10.3341/kjo.2008.22.4.220.
10. Holland SP, Morck DW, Lee TL. Review
update on toxic anterior segment syndrome.
Curr Opin Ophthalmol. 2007; 18(1): 4-8.
11. Kageyama T, Yaguchi S, Metori Y, et al.
Visual results and complications of temporal
incision phacoemulsification performed with
the non-dominant left hand by junior
ophthalmologists. Br J Ophthalmol. 2002;
86(11): 1222-1224.

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CAZURI CLINICE

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Jurnalul de Chirurgie (Iai), 2013, Vol. 9, Nr. 2

TRATAMENTUL PE CALE LAPAROSCOPIC N HERNIA


INGHINAL MULTIPL - PREZENTARE DE CAZ
Lucica Timiescu , Clarisa Gdea, N. Iordache
Clinica de Chirurgie General, Spitalul Clinic de Urgen Sf. Ioan, Bucureti, Romnia
LAPAROSCOPIC TREATMENT FOR MULTIPLE INGUINAL HERNIAS CASE REPORT
(Abstract): The miopectineal weak area described by Fruchaud is better visualized by
laparoscopic approach, and associated occult hernias of this region can be easily diagnosed, either
ipsilateral or contralateral. The goal of this paper is to emphasize the less obvious advantages of
mini-invasive approach, by a case study of a bilateral hernia (left inguinal hernia and recurrent
right inguinal hernia), operated by laparoscopic means using TEP (total extraperitoneal) approach.
A femoral hernia without clinical manifestations was diagnosed intraoperatively. All three hernias
were repaired during the same operation. The postoperative course was uneventful and the patient
was discharged three days after the procedure. CONCLUSIONS: The laparoscopic approach of
inguinal hernias offers the possibility to diagnose and to treat the occult inguinal hernias with low
rate of postoperative morbidity and recurrence.
KEY WORDS: GROIN HERNIA; OCCULT HERNIA; LAPAROSCOPY; TEP
SHORT TITLE: TEP n hernia inghinal multipl
TEP for multiple inguinal hernia
HOW TO CITE: Timiescu L, Gdea C, Iordache N. [Laparoscopic treatment for multiple inguinal hernia case report].
Jurnalul de chirurgie (Iai). 2013; 9(2): 167-171. DOI: 10.7438/1584-9341-9-2-8.

INTRODUCERE
Chiar dac abordul laparoscopic n
tratamentul herniilor inghinale se practic de
foarte muli ani, nu s-a impus drept gold
standard, aa cum s-a ntmplat cu
colecistectomia sau fundoplicatura gastric
laparoscopic [1].
Tratamentul pe cale laparoscopic al
herniilor inghinale ofer multiple avantaje:
reducerea durerii postoperatorii, complicaii
parietale mai puine, rat de recidiv mai
sczut i nu n ultimul rnd reducerea
duratei de spitalizare. n plus, laparoscopia
permite diagnosticarea herniilor neevidente
clinic, att ipsilaterale ct i controlaterale
[2,3].
Dac aceste hernii nediagnosticate
clinic ar fi lsate netratate, pacientul ar
continua s fie simptomatic sau ulterior ar fi
raportat ca avnd o recidiv [3].

PREZENTARE CAZ
Bolnavul L.T. n vrsta de 63 de ani sa internat n Clinica de Chirurgie a Spitalului
Sf Ioan Bucureti pentru o formaiune
pseudotumoral la nivelul regiunii inghinale
stngi i o alta la nivelul cicatricii
postoperatorii din regiunea inghinal
dreapt, ambele nsoite de durere local.
Simptomatologia pacientului a debutat
insidios n urma cu 4 ani, durerile fiind
asociate efortului fizic.
Din
antecedentele
personale
patologice, reinem o intervenie chirurgical
pentru hernie inghinal dreapt n urma cu 5
ani (procedeu anatomic), hipertensiune
arterial esenial stadiul II, controlat
medicamentos.
La examenul clinic pacientul avea o
stare general bun, afebril, prezentnd la
nivelul cicatricii de inghinotomie dreapt o

Received date: 19.11.2012


Accepted date: 30.12.2011
Adresa de coresponden: Dr. Lucica Timiescu,
Clinica de Chirurgie General, Spitalul Clinic de Urgen Sf. Ioan, Bucureti
oseaua Vitan Brzeti, nr. 13, sector 4, Bucureti, Romnia
Tel.: 0040 (0) 21 33 45 075
E-mail: lucia.timisescu@yahoo.com

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formaiune pseudotumoral, cu impulsiune i


expansiune la tuse, reductibil la taxis, iar n
regiunea inghinal stng o formaiune
pseudotumoral cu aceleai caracteristici.
Diagnosticul clinic a fost de hernie inghinal
dreapt recidivat i hernie inghinal oblic
extern stng.
Investigaiile paraclinice nu au
evideniat alte modificri patologice.
S-a
intervenit
chirurgical,
sub
anestezie general cu intubaie orotraheal,
prin abord laparoscopic extraperitoneal (TEP
- total extraperitoneal).
S-a disecat spaiul properitoneal cu
trocarul cu balona, care a fost ulterior
nlocuit cu altul de 12 mm cu sistem de
etaneizare i s-a insuflat CO2 la presiune de
10-12 mm Hg.
Dispoziia celor 3 trocare de lucru de 5
mm a fost astfel: unul la civa cm
subombilical i dou deasupra spinelor iliace
anterosuperioare, la 3-4 cm superior i 1-2
cm medial de acestea. S-a identificat, disecat
i redus un sac de hernie oblic extern pe
partea stng (Fig. 1) iar pe partea dreapt
un sac de hernie direct. Surpriza
intraoperatorie a fost c sub tractul ileopubic
drept s-a identificat, disecat i redus un sac
de hernie femural neidentificat la
examenul clinic (Fig. 2). S-au rulat i
introdus prin trocarul optic 2 proteze de
polipropilen monofilament, cu dimensiuni de
12 x 15 cm.
Protezele au fost simple, fr fant i
nu au necesitat fixare, ele urmnd s fie
meninute n poziie de ctre presiunea
intraperitoneal. Protezele au fost plasate
astfel nct s acopere ntreaga zon
slab inghinofemural (Fruchaud) pentru a
preveni formarea altor hernii [4] (Fig. 3).
Exsuflarea gazului s-a fcut progresiv,
sub control vizual, asigurndu-ne c
protezele au rmas corect poziionate pe
peretele muscular.
Evoluia
postoperatorie
a
fost
favorabil, pacientul fiind externat n a treia
zi postoperator.
Controalele periodice nu au semnalat
morbiditate postoperatorie sau recidiva
herniei la 6 luni, 1 an sau 2 ani postoperator.

Fig. 1 Sacul de hernie oblic extern stng

Fig. 2 Defectele parietale pe partea dreapt

Fig. 3 Aspect final dup plasarea celor dou proteze


de polipropilen

DISCUII
Hernia ocult este definit ca o hernie
care nu a fost identificat la examenul clinic
[3]. Acest lucru se poate ntmpla fie n
contextul coexistenei a dou defecte
herniare din care unul este evident, cellalt

TEP n hernia inghinal multipl

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Jurnalul de Chirurgie (Iai), 2013, Vol. 9, Nr. 2

scpnd examinatorului, fie cnd hernia


dei este simptomatic, are dimensiuni prea
mici pentru a putea fi evideniat clinic.
Missed hernia syndrome este definit
prin tratarea unui defect herniar izolat i
lipsa tratrii unei hernii inghinale ipsilaterale
coexistente datorit evalurii incomplete a
regiunii inghinofemurale [6]. O hernie
nediagnosticat clinic, sau trecut cu vederea
la intervenia chirurgical anterioar, poate fi
responsabil
pentru
simptomatologia
persistent [3].
Cele mai multe dintre aceste hernii
ratate la examenul clinic sau la intervenia
chirurgical sunt hernii femurale sau
obturatorii [2].
Unul
dintre
motivele
eecului
diagnostic este raritatea lor. n timp ce
hernia femural reprezint 2-8% din totalul
herniilor inghinale [7], hernia obturatorie
reprezint mai puin de 1% din totalul
herniilor
[8].
Uurina
stabilirii
diagnosticului clinic a herniei inghinale face
s scape diagnosticului, o hernie femural
concomitent.
Hernia femural prezint dificulti n
diagnostic mai mari dect alte hernii
abdominale externe [9]. Aceasta este o
afeciune mai frecvent la femei. La brbai,
herniile femurale sunt rare i, n mai mult de
jumtate din cazuri, sunt asociate cu o hernie
inghinal [10].
Diagnosticul de hernie inghinal poate
fi stabilit prin examenul clinic cu o
sensibilitate de 74,5-92% i specificitate de
93% [11-13]. Doar cazurile cu hernii
neevidente clinic/tumefacii abdominale
ndoielnice necesit investigaii suplimentare
de diagnostic [13-15].
n dubiile de diagnostic investigaia
iniial de elecie este ecografia parietal.
ntr-o analiz sistematic de evaluare a
herniiilor
oculte,
ultrasonografia
i
herniografia (peritoneografia) au fost cel mai
des utilizate [14]. Necesitatea de a
diagnostica i rezolva ct mai rapid
simptomatologia algic la sportivii de
performan a fcut s se dezvolte
investigaiile pentru diagnosticarea herniilor
oculte. Cu ajutorul herniografiei, au fost

diagnosticate hernii oculte n 25% din


cazuri, la sportivii care prezentau dureri
inghinale de lung durat fr a putea fi
definite anterior [16]. Computer tomografia
poate detecta majoritatea herniilor inghinale
care necesit intervenie chirurgical.
Rezonana magnetic nuclear (IRM) are
sensibilitate i specificitate de peste 94% n
diagnosticul herniilor inghinale i de
asemenea poate diagnostica alte afeciuni
asociate [13]. Costul i lipsa de
disponibilitate poate limita posibilitatea
practic a IRM.
Dei herniografia poate fi mai exact,
este invaziv i este rareori necesar, avnd
la dispoziie alte investigaii noninvazive
[17,18]. n cazul n care imagistica nu
reuete s identifice o hernie suspectat,
laparoscopia diagnostic poate fi folosit
pentru a evidenia sau exclude definitiv o
hernie [5]. Intervenia chirurgical pe cale
laparoscopic ofer oportunitatea de a
examina toate orificiile herniare inghinale i
de a identifica defectele parietale pierdute
la examenul clinic sau interveniile
chirurgicale anterioare [1,4,19].
La o proporie semnificativ de
pacieni operai pe cale laparoscopic, s-a
pus n eviden o hernie femural asociat
herniei inghinale, literatura de specialitate
raportnd o inciden de 6-33% [20-22].
Aceste hernii concomitente sunt uor tratate
n aceeai edin operatorie laparoscopic.
Ekberg et al., ntr-un studiu pe 314 pacieni
cu hernii inghinale, a artat c 71 pacieni
(23%) au avut hernii multiple [3].
O situaie clinic aparte este hernia
femural, dup cura chirurgical a herniei
inghinale. Cauza este fie o hernie ignorat,
fie o hernie secundar herniorafiei inghinale.
Herniile ignorate apar dup intervenii
chirurgicale pe cale anterioar dac regiunea
femural nu este explorat [23]. ntr-un
studiu pe 34.849 cazuri de hernie inghinal
operat, Mikkelsen et al. [24] constat o
inciden de 15 ori mai mare a herniei
femurale dup herniorafia inghinal (cu/fr
protez), comparativ cu incidena spontan.
Aceste recidive femurale au aprut mai
devreme dect recidivele inghinale, sugernd

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c foarte probabil sunt hernii trecute cu


vederea la prima operaie [24]. Mikkelsen et
al. consider c trebuie explorat de rutin
canalul femural n timpul curei chirurgicale
a herniei inghinale [24].
O alt explicaie ar fi c operaia
precedent de hernie inghinal poate
precipita formarea unei hernii femurale [24].
Aceasta se poate datora traciunii ascendente
asupra tractului ileopubic i lrgirii
consecutive a canalului femural [4,23].
Pentru herniile recidivate dup
interveniile pe cale anterioar, laparoscopia
pare s aib avantaje clare, deoarece este
abordat un alt plan de disecie i de
implantare a protezei [1,13].
Pe lng aceste hernii concomitente
ipsilateral,
n
cursul
interveniilor
chirurgicale
laparoscopice
pot
fi
diagnosticate i herniile controlaterale care
nu au expresie clinic. Incidena herniilor
oculte controlaterale astfel identificate este
ntre 10-20% [25]. Un studiu realizat de
Crawford et al, a artat c 37 din 73 de
pacieni (50%) au avut hernie bilateral
diagnosticat laparoscopic [2].
Atunci cnd este diagnosticat o hernie
femural, intervenia chirurgical trebuie
planificat ct mai repede chiar dac
simptomele sunt absente, datorit riscului
crescut de trangulare.
Ratele de recidiv dup cura
chirurgical a herniei inghinale variaz ntre
3-20% [3]. O parte din procentaj poate fi
imputat herniilor ipsilaterale concomitente.
Cele mai multe recidive dup cura
chirurgical aloplastic a herniilor inghinale
apar n timpul primului an de la operaie i
sunt secundare unor defecte de tehnic
chirurgical sau secundare unor complicaii,
cum ar fi infecia i hematomul [6].
CONCLUZII
Tratamentul pe cale laparoscopic
permite diagnosticarea herniilor inghinale i
femurale concomitente, oculte clinic, precum
i rezolvarea lor simultan, fr morbiditate
supra-adugat, reducnd n acest fel
incidena recidivelor i a simptomatologiei
persistente cauzat de herniile oculte.

CONFLICT DE INTERESE
Autorii nu declar nici un conflict de
interese.

BIBLIOGRAFIE
1. Moldovanu R, Pavy G. Laparoscopic
transabdominal pre-peritoneal (TAPP) for
bilateral inguinal hernia. Jurnalul de chirurgie
(Iai). 2010; 6(3): 373-382.
2. Crawford DL, Hiatt JR, Phillips EH.
Laparoscopy identifies unexpected groin
hernias. Am Surg. 1998; 64(10): 976978.
3. Ekberg O, Lasson A, Kesek P, Van Westen D.
Ipsilateral multiple groin hernias. Surgery.
1994; 115(5): 557562.
4. Trcoveanu E, Bradea C, Moldovanu R.
[Anatomy of the inguinal region]. Jurnalul de
chirurgie (Iai). 2005; 1(4): 436-446.
5. Dulucq JL, Wintringer P, Mahajna A. Occult
hernias detected by laparoscopic totally extraperitoneal inguinal hernia repair: a prospective
study. Hernia. 2011; 15(4): 399-402.
6. Lowham AS, Filipi CJ, Fitzgibbons RJ Jr,
Stoppa R, Wantz GE, Felix EL, Crafton WB.
Mechanisms of hernia recurrence after
preperitoneal mesh repair. Traditional and
laparoscopic. Ann Surg. 1997; 225(4): 422
431.
7. Hachisuka T. Femoral hernia repair. Surg Clin
North Am. 2003; 83(5): 11891205.
8. Wu J-M, Lin H-F, Chen K-H, Tseng L-M,
Huang S-H. Laparoscopic preperitoneal mesh
repair of incarcerated obturator hernia and
contralateral direct inguinal hernia. J
Laparoendosc Adv Surg Tech A. 2006; 16(6):
616-619.
9. Naude GP, Ocon S, Bongard F. Femoral
hernia: the dire consequences of a missed
diagnosis. Am J Emerg Med. 1997; 15(7):
680682.
10. Mathonnet M, Mehinto D. Femoral hernias:
repair techniques. J Chir (Paris). 2007; 144
Spec No 4: 5S15-8.
11. Van den Berg JC, De Valois JC, Go PM,
Rosenbusch G. Detection of groin hernia with
physical examination, ultrasound, and MRI
compared with laparoscopic findings. Invest
Radiol. 1999; 34(12): 739743.
12. Kraft BM, Kolb H, Kuckuk B, Haaga S, Leibl
BJ, Kraft K, et al. Diagnosis and classification
of inguinal hernias. Surg Endosc. 2003;
17(12): 20212024.
13. Simons MP, Aufenacker T, Bay-Nielsen M,
Bouillot JL, Campanelli G, Conze J, et al.
European Hernia Society guidelines on the
treatment of inguinal hernia in adult patients.
Hernia. 2009; 13(4): 343-403.

TEP n hernia inghinal multipl

171
Jurnalul de Chirurgie (Iai), 2013, Vol. 9, Nr. 2

14. Robinson A, Light D, Kasim A, Nice C. A


systematic review and meta-analysis of the role
of radiology in the diagnosis of occult inguinal
hernia. Surg Endosc. 2013; 27(1):11-18.
15. Sayad P, Abdo Z, Cacchione R, Ferzli G.
Incidence of incipient contralateral hernia
during laparoscopic hernia repair. Surg
Endosc. 2000; 14(6): 543545.
16. Kesek P, Ekberg O, Westlin N. Herniographic
findings in athletes with unclear groin pain.
Acta Radiol. 2002; 43[6]: 603608.
17. Hamlin JA, Kahn AM. Herniography: a
review of 333 herniograms. Am Surg. 1998;
64(10): 965969.
18. Hall C, Hall PN, Wingate JP, Neoptolemos JP.
Evaluation of herniography in the diagnosis of
an occult abdominal wall hernia in
symptomatic adults. Brit J Surg. 1990; 77(8):
902906.
19. Oprea V, Gavrilas F. Chirurgia peretelui
abdominal - vol II Hernia inghinal
recidivat. Hernia incizional. Cluj Napoca:
Editura Universitar Iuliu Haieganu 2010.

20. Hernandez-Richter T, Schardey HM, Rau HG,


Schildberg FW, Meyer G. The femoral hernia:
an ideal approach for the transabdominal
preperitoneal technique [TAPP]. Surg Endosc.
2000; 14(8): 736740.
21. Garg P, Ismail M. Laparoscopic total
extraperitoneal repair in femoral hernia
without fixation of the mesh. JSLS. 2009;
13(4): 597600.
22. Felix EL, Michas CA, Gonzalez MH.
Laparoscopic hernioplasty: Why does it work?
Surg Endosc. 1997; 11(1): 3641.
23. Chan G, Chan C-K. Longterm results of a
prospective study of 225 femoral hernia
repairs: indications for tissue and mesh repair.
J Am Coll Surg. 2008; 207(3): 360367.
24. Mikkelsen T, Bay-Nielsen M, Kehlet H. Risk
of femoral hernia after inguinal herniorrhaphy.
Brit J Surg. 2002; 89(4): 486488.
25. Quilici PJ, Greaney EM, Quilici J, Anderson
S. Transabdominal preperitoneal laparoscopic
inguinal herniorrhaphy: results of 509 repairs.
Am Surg. 1996; 62(10): 849-852.

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Timiescu L. et al.

CASE REPORT

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THYMOMA WITH LATERAL AND PARACARDIAC


EVOLVEMENT
Oana-Raluca Lucaciu1 , P.V-H. Boianu1, T. Hogea1,
Claudia Dorob2, A-M. Boianu1
1) Department of Surgery, University of Medicine and Pharmacy Tg. Mure, Romania
2) Department of Radiology, Emergency Clinic County Hospital Tg. Mure, Romania
THYMOMAS WITH LATERAL AND PARACARDIAC EVOLVEMENT (Abstract): Thymoma
is the most common tumor of the anterior mediastinum originating from epithelial thymic cells.
The tumors are often asymptomatic or with non specific symptoms. We present herein three cases
admitted in our surgical for mediastinal tumor. The imagery exams revealed thymomas with
lateral and paracardiac evolvement. Intraoperatively, we found tumors in closed contact with the
pericardium, developed posterior to the phrenic nerve. In all cases, we performed complete
excision of the tumors using a posterolateral thoracotomy. Frozen section was inconclusive in all
cases; the final pathological exam diagnosed stage I thymoma. The postoperative course was
uneventful for all three patients. The long term follow-up (14 years) revealed no recurrence.
KEY WORDS: THYMOMA; MEDIASTINAL TUMORS; THORACOTOMY.
SHORT TITLE: Lateral & paracardiac thymoma
HOW TO CITE: Lucaciu OR, Boianu PVH, Hogea T, Dorob C, Boianu AM. Thymoma with lateral and paracardiac,
evolvement. Jurnalul de chirurgie (Iai). 2013; 9(2): 173-178. DOI: 10.7438/1584-9341-9-2-9.

INTRODUCTION
Thymoma is a tumor originating from
epithelial thymus cells, the thymocytes [1].
Most often it is located in anterior
mediastinum (95%); other sites as cervical
region, pulmonary hilar regions, lung
parenchyma,
visceral
mediastinum,
cardiophrenic angle, paravertebral sulcus,
tracheal wall (like a tracheal polyp
appearance) are also noted [2].
Thymoma is often asymptomatic and
diagnosed incidentally during a routine
thoracic X-ray exam or associated with signs
of mediastinal compression (superior vena
cava syndrome, dysphagia, dyspnea, chest
pain); in 30 to 45% it is associated with
myasthenia gravis [2].
During the last 15 years we had 3
cases referred to our unit with the diagnosis
of mediastinal / pulmonary tumor, where the
preoperative imagery showed a mediastinal
tumor, with lateral-paracardiac evolvement.

Case 1
A 47 years old woman was admitted in
our service for chest pain, medium dyspnea
and irritating cough. The symptoms started
three months before. On admission, physical
exam found no other pathological aspects.
The thoracic X-ray exam showed a round
opacity in the upper chest, over the
heart near the intersection with large vessels
(Fig. 1). Computed tomography (CT)
showed a solid mass in the superior
mediastinum, well defined, encapsulated;
ultrasound exam revealed no pericardial and
pleural fluid.
After conducting interdisciplinary
preoperative pulmonology and cardiology
checkups
and achieving a proper
preoperative preparation, the surgical
intervention was performed under general
anaesthesia with orotracheal intubation.
Intraoperatively, we performed a
posterolateral thoracotomy that gave us an

Received date: 12.03.2013


Accepted date: 23.03.2013
Correspondence to: Oana-Raluca Lucaciu, MD
Str. George Cobuc, no. 11/9, 540119, Tg. Mure, Mure County, Romania
Phone: 0040 (0) 745 54 37 76
E-mail : lucaciuoanaraluca@yahoo.com

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excellent exposure; we found a well


delimitated and encapsulated tumor in closed
contact with the pericardium, developed
posterior to the phrenic nerve and we
performed the complete tumor removal.
The patient postoperative course was
uneventful and was discharged after 10 days.
The follow-up revealed no recurrence during
6 years after the surgical procedure.
Frozen histopathological examination
was inconclusive; the diagnosis was made
by final histopathology that showed no
atypical cells - stage Masaoka I.

Fig. 1 Case 1: Thoracic X-ray exam: opacity in


superior mediastinum

Fig. 2 Case 2: CT scan: solid mass in anterior


mediastinum with lateral and paracardiac evolvement

Fig. 3 Case 2: Resected secimen

Case 2
A 70 years old woman was admitted in
our surgical unit for irritating dry cough,
dyspnea, hoarseness, night sweats and pain
in the right hemithorax. The thoracic X-ray

exam revealed opacity in the lower half of


the chest with extension to the straight
hemithorax.
The CT scan shows a solid mass in the
anterior
mediastinum
well
defined,
encapsulated, developed posterior to the
phrenic nerve (Fig. 2).
Surgical excision was made using also
a posterior lateral thoracotomy, with the
complete removal of the tumor (Fig. 3).
The postoperative course was also
uneventful and the patient was discharged
day 14th. No recurrence has been noted 14
years after surgical procedure. The
pathological exam showed no atypical cells
(stage Masaoka I).
Case 3
A 46 years old woman was admitted in
our surgical department for non specific
symptoms: diffuse chest pain, irritating dry
cough and loss of appetite. From shes past
medical history we noted the hysterectomy
performed 5 years ago. On admission,
physical exam found no other pathological
aspects.
Thoracic X-ray exam showed an oval
opacity in the lower half of the chest with
extension to the right hemithorax (Fig. 4).
CT scan confirmed a well defined,
encapsulated, solid mass, without pericardial
and pleural fluid (Fig. 5).
After conducting interdisciplinary
preoperative pulmonology and cardiology
and oncological checkups, and achieving a
proper preoperative preparation, the surgery
was performed under general anaesthesia
with orotracheal intubation.
We performed an antero-lateral
thoracotomy; a well delineated and
encapsulated tumor in close contact with the
pericardium was found and the complete
removal of the tumor was performed
(Fig. 6).
Frozen sections were inconclusive; the
pathological exam revealed lymphocyte cell
thymoma (stage Masaoka I).
The
postoperative
course
was
uneventful and we have not met any
recurrence after 9 years.

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Fig. 4 Case 3: Oval opacity in the lower half of the


chest with extension to the right hemithorax

Fig. 5 Case 3: Lateral and paracardiac tumor

Fig. 6 Case 3: Resected specimen

DISCUSSION
Thymoma, the most common tumor of
the mediastinum represents 20-25% of all
mediastinal tumors and 50% of overall
mediastinal masses [5]. Maximum incidence
of thymoma is in the fourth or fifth decade

of life; the patients average age is 52 [5].


The incidence is similar in women and in
men [5]. In our study, all cases were women
averaging 54.3313.33 years old.
Although
the
development
of
thymoma in childhood is rare, the symptoms
are more frequent in children than in adults
[6].
About 50% of patients with thymoma
are asymptomatic [7]. Non specific
symptoms are noted like chest pain, cough
and dyspnea [7]. More severe symptoms
such as superior vena cava syndrome,
phrenic nerve paralysis or recurrent
laryngeal nerve paralysis that causes raucous
voice are rare and most frequently indicates
malignancy of the lesion [6]. Chest wall or
pleural invasion can also occur in the case of
amalignant
thymoma,
frequently
accompanied by persistent pleural effusion
and significant local pain [6].
Other general signs associated with
thymoma are weight loss, fever, fatigability
and night sweats and were present in 20% of
patients included [7].
Myasthenia gravis is a relatively rare
disease and can occur at any age. Women
are affected more frequently than men, with
peak incidence around 30 years old; the peak
incidence in men is reached at the age of 5060 years. Surgical treatment of myasthenia is
the thymectomy. Remission rate increases in
time reaching 40-60% at 7-10 years after the
surgery [2].
Posteroanterior (PA) and lateral chest
X-ray exams can detect most of thymomas.
On the PA view, the lesion typically appears
as a smooth mass in the upper half of the
chest, overlying the superior portion of the
cardiac shadow near the junction of the heart
and great vessels. The mass usually projects
predominantly into one of the hemi thoraces.
On the right side, the silhouette sign is
present and the ascending portion of the
aortic arch is obliterated. Conversely, if the
thymoma is on the left side, the silhouette
sign is obscured and the aortic knob is
identified behind the mass [7].
CT scan may delineate a mass further
or detect a smaller tumor missed on

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radiography. CT scan is the gold standard


imaging procedure in patients with miastenia
gravis. Thymic enlargement should be
determined because most enlarged thymus
glands on CT scan represent a thymoma. CT
scanning with intravenous contrast dye is
mandatory and shows the relationship
between thymoma and surrounding vascular
structures; it also defines the vascularity
pattern and assists the surgeon to plan the
surgical procedure to completely remove the
tumor [7].
Positron emission tomography (PET)
has proven to be invaluable in confirming
the diagnosis of malignant invasive
thymoma. Although CT may reveal evidence
of anterior mediastinal masses, PET scan
shows the hypermetabolic activity, thus the
suspicion of malignancy. PET should be
added as a diagnosis method to help the
surgeon in determining the adequate stage
and involvement of other structures [8].
Preoperative histological diagnosis can
be
achieved
through
biopsy
by
mediastinoscopy, thoracoscopy or CT
guided transparietal biopsy [9].
With reference to histology, there is no
clear distinction between benign or
malignant thymoma. The trend of a benign
or malignant thymoma is determined by its
invasive character. Malignant thymoma
invades the great vessels, lymphatics and
adjacent areas of the mediastinum structures.
The survival rate of people with invasive
thymoma for a 15 year-period is 12.5% and
47% for a person with non-invasive
thymoma. Death usually occurs by cardiac
tamponade or other cardio-respiratory
complications [10].
Usually thymoma are classified using
Masaoka Staging System (Table I) [3].
The histological type is also essential
for the prognosis; so, for medullary and
mixed thymoma the disease free survival
rate is 100% and decreased to 28% for
thymic carcinoma (Table II) [4,5].
Several reports from the literature
suggest that benign or malignant thymomas
are chemosensitive tumors. Potential
candidates for chemotherapy include

approximately one third of the patients with


invasive thymoma, metastasis and all
patients with stage IV disease. Fornasiero A
et al. [5] reported successful long-term
survival following treatment with cisplatin +
vincristine
+
doxorubicin
+
cyclophosphamide for invasive Thymoma
incompletely resected or inoperable cases.
Out of 32 patients, 90% have responded to
therapy with a mean survival of 15 months.
A study performed by the European
Organisation for Research and Treatment of
Cancer reported that in 16 cases of patients
with recurrent or metastatic thymoma, were
observed five complete remissions and four
partial remissions. The median survival in
this study was 4.3 years. [11]
Table I Masaoka Staging System of thymomas [3]
Stage
I

II

III
IVA
IVB

Definition
Encapsulated tumor
with no gross or
microscopic invasion
Macroscopic invasion
into the mediastinal
fat or pleura or
Microscopic invasion
into the capsule
Invasion of the
pericardium, great
vessels, or lung
Pleural or pericardial
metastatic spread
Pleural or pericardial
metastatic spread

Treatment
R0 surgical
excision

R0 surgical
excision + RT

R0 surgical
excision + RT
Surgical debulking
+ RT + CHT
Surgical debulking
+ RT + CHT

RT radiotherapy; CHT chmiothrapy

Table II World Health Organization: thymoma pathologic


classification [4,5]

Type

Histologic Description

DFS (%)

Medullary thymoma

100

AB

Mixed thymoma

100

B1

Predominantly cortical thymoma

83

B2

Cortical thymoma
Well-differentiated thymic
carcinoma
Thymic carcinoma

83

B3
C

35
28

DFS: 10 years Disease-Free Survival rate

Case reports have documented the use


of oral corticosteroids causing regression of
an invasive thymoma [12]. In one case, the

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patient showed complete regression of the


thymoma and associated symptoms without
radiological recurrence after 12 months
[12,13].
The initial stage of treatment in most
cases of the thymoma is surgery. Surgical
resection is the treatment of choice for most
neoplasms arising in the mediastinum. In
cases of benign lesions the tumor complete
excision is generally sufficient. Thymoma is
one of the exceptions from this principle
because total thymectomy is indicated for all
benign or malignant thymoma; the tumor has
to be resected without breaking the
capsule. Surgical excision provides tissue for
histological examinations and information
on the invasive character of the tumor,
which is important to determine the need for
an adjuvant therapy. In cases of malignant
thymomas, a complete R0 resection should
be performed. Pericardium, pleura, lung
segments, sternum, ribs and diaphragm can
be resected to achieve R0 resection in the
cases with invasive thymomas [16].
Furthermore brachiocephalic vein and even
superior vena cava can be resected; the
vascular reconstruction is usually performed
using prosthetic grafts [17,18].
The surgery approach is the mid line
sternotomy or posterolateral thoracotomy; in
invasive
thymoma
for
multivisceral
resections the transverse sternotomy
extended in 4th intercostals space could be
necessary. The video assisted resection is
accepted for stage I disease [19].
A single-institution retrospective study
was conducted involving 5 patients with
stage
IVA
treated
with
pleurapneumonectomy [20]. The median survival
was 86 months, and the Kaplan-Meier
survival was 75% at 5 years and 50% at 10
years. There were no operative mortalities in
this study. It has been suggested that, in
selected patients, this approach, the complete
resection after neoadjuvant chemotherapy,
may be promising [20].
A multidisciplinary approach to the
treatment for inoperable thymoma was also
developed. In a study conducted by the MD
Anderson Cancer Center, a regimen

consisting of the induction chemotherapy,


surgical
resection,
postoperative
radiotherapy,
and
consolidation
chemotherapy
(e.g.
3
cures
of
cyclophosphamide, doxorubicin, cisplatin,
and prednisone) was tested. [14,15]
CONCLUSIONS
The prognosis of thymoma depends on
tumor histology. The presented cases were
Masaoka I stage tumors. The tumors were
completely removed and the outcome of the
patients was very good with no recurrences
for up to 14 years. The lateral approach
provides good access and facilitates the
resection.
CONFLICT OF INTERESTS
None to declare
ACKNOWLEDGEMENT
This paper is partly supported by the
Sectorial Operational Programme Human
Resources Development (SOP HRD),
financed from the European Social Fund and
by the Romanian Government under the
contract number POSDRU 80641.
REFERENCES
1. Detterbeck FC, Parsons AM. Thymic tumors.
Ann Thorac Surg. 2004; 77(5): 1860-1869.
2. Mullen B, Richardson JD. Primary anterior
mediastinal tumors in children and adults. Ann
Thorac Surg. 1986; 42(3): 338-345.
3. Falkson CB, Bezjak A, Darling G, et al. The
management of thymoma: a systematic review
and practice guideline. J Thorac Oncol. 2009;
4(7): 911-919.
4. Kondo K, Yoshizawa K, Tsuyuguchi M, et al.
WHO histologic classification is a prognostic
indicator in thymoma. Ann Thorac Surg. 2004;
77(4): 1183-1188.
5. Fornasiero A, Daniele O, Ghiotto C, et al.
Chemotherapy for invasive thymoma. A 13year experience. Cancer. 1991; 68(1): 30-33.
6. Konstantinov IE, Saxena P, Koniuszko M, et
al. Superior vena cava obstruction by tumor
thrombus in invasive thymoma: diagnosis and
surgical management. Heart Lung Circ. 2007;
16(6):462-464.
7. Blumberg D, Port JL, Weksler B, et al.
Thymoma: a multivariate analysis of factors
predicting survival. Ann Thorac Surg. 1995;
60(4): 908-913; discussion 914.

178

Lucaciu OR. et al.

Jurnalul de Chirurgie (Iai), 2013, Vol. 9, Nr. 2

8. Bagga S, Bloch EM. Imaging of an invasive


malignant thymoma on PET Scan: CT and
histopathologic correlation. Clin Nucl Med.
2006; 31(10): 614-616.
9. Wilkins EW, Grillo HC, Scannell JG,
Moncure AC, Mathisen DJ. J. Maxwell
Chamberlain Memorial Paper. Role of staging
in prognosis and management of thymoma.
Ann Thorac Surg. 1991; 51(6): 888-892.
10. Wu KL, Mao JF, Chen GY, et al. Prognostic
predictors and long-term outcome of
postoperative irradiation in thymoma: a study
of 241 patients. Cancer Invest. 2009; 27(10):
1008-1015.
11. Okumura M, Ohta M, Tateyama H, et al. The
World Health Organization histologic
classification system reflects the oncologic
behavior of thymoma: a clinical study of 273
patients. Cancer. 2002; 94(3): 624-632.
12. Barratt S, Puthucheary ZA, Plummeridge M.
Complete regression of a thymoma to
glucocorticoids, commenced for palliation of
symptoms. Eur J Cardiothorac Surg. 2007;
31(6): 1142-1143.
13. Fujiwara T, Mizobuchi T, Shibuya K,
Hiroshima K, Fujisawa T, Iwai N. Rapid
regression of stage IVb invasive thymoma
under palliative corticosteroid administration.
Gen Thorac Cardiovasc Surg. 2007; 55(4):
180-183.

14. Shin DM, Walsh GL, Komaki R, et al. A


multidisciplinary approach to therapy for
unresectable malignant thymoma. Ann Intern
Med. 1998; 129(2): 100-104.
15. Engels EA, Pfeiffer RM. Malignant thymoma
in the United States: demographic patterns in
incidence and associations with subsequent
malignancies. Int J Cancer. 2003; 105(4): 546551.
16. Dango S, Passlick B, Thiemann U, et al. The
role of a pseudocapsula in thymic epithelial
tumors: outcome and correlation with
established prognostic parameters. Results of a
20-year single center retrospective analysis. J
Cardiothorac Surg. 2009; 4(1): 33.
17. Gonzalez M, Krueger T, Perentes JY,
Matzinger O, Peters S, Ris HB. Extrapleural
pneumonectomy with venous confluence
resection for stage IVA thymic tumors. Ann
Thorac Surg. 2011; 91(3): 941-943.
18. Arvind K, Roman D, Umashankkar K, Pramod
KJ, Shiv KC, Neeti M. Resection and
reconstruction of mediastinal great vessels in
invasive thymoma. Indian J Cancer. 2010;
47(4): 400-405.
19. Venuta F, Anile M, Diso D, et al. Thymoma
and thymic carcinoma. Eur J Cardiothorac
Surg. 2010; 37(1): 13-25.
20. Wright CD. Pleuropneumonectomy for the
treatment of Masaoka stage IVA thymoma.
Ann ThoracSurg. 2006; 82(4):1234-1239.

CAZURI CLINICE

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MIASTENIA GRAVIS POST-TIMECTOMIE


C. Mota, Natalia Mota, T. Horvat
Clinica de Chirurgie Toracic, Institutul Oncologic Prof. Dr. Al. Trestioreanu Bucureti
Universitatea de Medicin i Farmacie Carol Davila, Bucureti

MIASTENIA GRAVIS AFTER THYMECTOMY (Abstract): Although the relationship between


myasthenia gravis and thymomas it is well known, with some of myasthenias disappearing after
thymectomy, myasthenia may develop after thymoma resection. We present a case of 36 years old
man who developed generalized myasthenia 6 years after thymoma surgery; it had been
performed tumorectomy, mediastinal fat resection, resection of the anterior wall of left
brachiocefalic vein with PTFE patch reconstruction (Masaoka stage III thymoma). After 4 years
of corticoid therapy (methylprednisolone) he was operated for steroid cataract. 11 years after
resection he is tumor-free and the brachiocefalic vein is functional on CT-scan. Myasthenia after
thymectomy is rare but possible after thymoma resection; it is not influenced by association of
mediastinal fat resection. The titer of specific auto antibodies and the grade of thymoma invasion
are predictive factors for myasthenia development after thymectomy.
KEY WORDS: MIASTENIA GRAVIS; THYMOMA; THYMECTOMY
SHORT TITLE: Miastenia gravis post timectomie
Myasthenia gravis after thymectomy
HOW TO CITE: Mota C, Mota N, Horvat T. [Myasthenia gravis after thymectomy]. Jurnalul de chirurgie (Iai). 2013;
9(2): 179-184. DOI: 10.7438/1584-9341-9-2-10.

INTRODUCERE
Miastenia gravis (MG) este o boal
autoimun a sinapsei neuromusculare, care
se caracterizeaz printr-o oboseal excesiv
a musculaturii striate, ce apare la efort i se
recupereaz parial sau total prin repaus sau
sub aciunea unor substane anticolinesterazice. Timoamele sunt tumori
maligne care deriv din esutul epitelial
timic.
Att miastenia ct i timoamele sunt
leziuni rar ntlnite n practica curent:
miastenia gravis apare cu o frecven anual
de 0,25-2 cazuri/100.000 locuitori [1], n
timp ce n cazul timoamelor frecvena anual
este de 0,15 cazuri/100.000 locuitori [2],
adic 0,2-1,5% din totalitatea tumorilor
maligne.
Este binecunoscut relaia dintre
timoame i miastenia gravis: 10-15% din
miastenii pot coexista cu un timom i,

invers, circa 30% din timoame pot prezenta


ca manifestare paraneoplazic miastenia
gravis [3].
Dei mecanismul fiziopatologic al
miasteniei nu este nc bine cunoscut, rolul
timusului este ns unanim acceptat. Pe alt
parte o manifestare paraneoplazic anun i
nsoete o malignitate i de multe ori se
remite dup exereza complet a leziunii
tumorale. La prima vedere este paradoxal ca
o paraneoplazie, care apare n strns
legtur cu un organ transformat malign, s
apar la mult vreme dup ce organul
respectiv i implicit tumora au fost extirpate.
Miastenia postoperatorie este definit ca
forma de miastenie gravis care apare dup
rezecia unui timom non-miastenic.
PREZENTARE DE CAZ
Pacientul D.S., la vrsta de 36 de ani,
n 2001, n urma unui examen radiologic de

Received date: 11.01.2013


Accepted date: 15.03.2013
Adresa de coresponden: Dr. Cezar Mota
Aleea Compozitorilor, nr.15, bloc 821, sc. A, ap. 39, sector 6, Bucureti, Romania
Tel.: 0040 (0) 744 63 87 03
E-mail: cezarmotas@gmail.com

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rutin, a fost diagnosticat cu o opacitate la


nivelul mediastinului. Examenul CT toracic
a confirmat existena unei formaiuni
tumorale n mediastinul anterior (Fig. 1, 2).
Iniial s-a adresat unui alt serviciu
chirurgical toracic unde s-a practicat o
mediastinotomie
anterioar.
Rezultatul
examenului histopatologic al fragmentelor
recoltate a fost timom. Ulterior s-a adresat
clinicii noastre. Preoperator, pacientul era
complet asimptomatic, nefiind evideniate
semne clinice ale miasteniei gravis. Nu s-au
dozat anticorpii antireceptor de acetilcolin
i nu s-au efectuat studii electromiografice.

Fig. 1 Radiografie toracic preoperatorie: lrgirea


discret a opacitii mediastinale

Fig. 2 Computer tomografie toracic cu substan de


contrast: se constat invazia timomului n trunchiul
venos brahiocefalic n apropierea vrsrii n vena
cav superioar

S-a
intervenit
chirurgical
prin
sternotomie median total i intraoperator
s-a decelat o voluminoas formaiune
tumoral timic ce invada trunchiul venos
brahiocefalic stng (TVBCS) i ambele
pleure mediastinale. S-a practicat rezecia
tumorii mediastinale n bloc cu timusul i
ntreaga grsime a mediastinului anterior. A
fost necesar rezecia pleurelor mediastinale
invadate i a circa 3 cm din peretele anterior
al trunchiului venos brahiocefalic invadat.
Reconstrucia vascular a fost efectuat cu
un petec de PTFE (Poli-Tetra-Fluor-Etilen).
Datorit manevrelor de eliberare a nervului
frenic drept din tumor s-a instalat o parez
tranzitorie a hemidiafragmului drept.
Aceasta a fost obiectivat de radiografia
postoperatorie i tradus clinic prin
necesitatea meninerii suportului ventilator
pentru primele 48 de ore postoperatorii.
Examenul histopatologic al piesei de rezecie
a fost de timom tipul AB (conform
clasificrii OMS) i, prin confirmarea
histopatologic a invaziei vasculare, tumora
a fost clasificat ca fiind n stadiul III
Masaoka.
Perioada postoperatorie a decurs fr
alte incidente, pacientul fiind externat la 11
zile de la intervenie cu recomandarea
continurii tratamentului anticoagulant. A
urmat tratament adjuvant (radioterapie i
chimioterapie) fiind dispensarizat n reeaua
oncologic. La jumtatea anului 2002
pacientul ncheie radioterapia mediastinului
i chimioterapia.
Evoluia n continuare a fost fr
incidente pentru ca, dup 6 ani, s se
instaleze relativ brusc astenia fizic
generalizat. Pacientul este diagnosticat cu
miastenia gravis grupa III Osserman, boala
fiind controlat prin tratament cu
anticolinesterazice (mestinon 4 x 60 mg/zi)
i antiinflamatoare steroidiene (metilprednisolon). Nivelul seric al anticorpilor
antireceptor de acetilcolin au avut valori de
84 nmol/L. Dup 4 ani de corticoterapie, n
2011, pacientul este operat pentru cataract
cortizonic. Ultimul control CT efectuat n
2010 nu relev semne de recidiv tumoral
sau alte localizri ale leziunii maligne. n

Miastenia gravis post timectomie

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plus demonstreaz permeabilitatea grefei


vasculare (Fig. 3).

Fig. 3 CT postoperator: absena recidivei tumorale i


permeabilitatea segmentului venos protezat

DISCUII
Miastenia gravis postoperatorie a fost
semnalat nc din anii 50, n acel moment
considerndu-se c aceasta ar fi legat de
recidiva tumoral [4,5]. Ulterior, majoritatea
raportrilor apariiei fenomenelor miastenice
au fost fcute n special la pacieni fr
recidiv tumoral, att n raportri solitare

[6,7] ct i n evaluri ale unor grupuri mai


mari de studiu [8-10].
n general frecvena apariiei acestor
manifestri este extrem de redus, fiind
rezultatul combinaiei a dou afeciuni rare.
Exceptnd 2 studii care raporteaz frecvene
de 28% (7 din 25) [8] i de 19,8% (9 din 46)
[11] din totalitatea timoamelor rezecate,
majoritatea autorilor cifreaz posibilitatea
apariiei acestei complicaii la valori
cuprinse ntre 1 i 11,8 % [3,12-14]. Valorile
mari obinute de Namba i colab. [8] trebuie
analizate i prin prisma lotului analizat: din
cei 72 de pacieni cu timom, 47 aveau i
miastenie n momentul operator (65,2%),
valorile fiind cu mult mai mari dect
raportrile generale ale asociaiei timom
miastenie (30%). De altfel, Namba i colab.
[8], integrnd cele 7 cazuri personale cu alte
26 de cazuri din alte studii, gsete o
frecven de 3% a miasteniei posttimomectomie. n Tabelul I sunt prezentate
sintetic cele mai reprezentative lucrri cu
privire la miastenia postoperatorie.
Majoritatea studiilor nu gsesc
corelaii ntre rata apariiei miasteniei
postoperatorii i forma histologic O.M.S.
[3,8,9,14], distribuia pe formele histologice
ale timomului rezecat fiind similar cu cea
ntlnit n timoamele cu miastenie n
momentul operaiei.

Tabel I Principalele studii referitoare la miastenia gravis post-timectomie


Studiul
Namba T, 1978 [8]
Ohta I, 1991[11]
Ito M, 1992 [13]
Evoli A, 2002 [10]
Li J, 2004 [14]
Kondo K, 2005 [3]
Nakajima J, 2008 [9]
Sun X, 2011[12]

n*
7 din 25
(28%)
9 din 46
(19,6%)
18 din 394
(4,6%)
13 din 207
(6,28%)***
15 din 127
(11,8%)
8 din 827
(1%)
5 din 55
(9%)
6 din 125
(4,8%)

AAC preoperator**

Recuren metastaze

2 spt. 6 ani

9 zile 5,8 ani

AAC antimusculatur
striat 9 din 18 (50%)

0 11 ani

5 recurene/11 cu
debut > 6 luni (45,4%)

6 luni 10 ani

3 recurene (23%)

0 137 luni

6 zile 45 luni

1 din 4 (25%)

3 46 luni

ARAch 3 din 13 (23%)

1 recuren (20%)

1spt. 31 luni

ARAch 4 din 22 (18,1%)

* Numrul pacienilor cu miastenie postoperatorie raportat la numrul timoamelor non-miastenice; ** Raportul dintre numrul pacienilor
miastenici cu titru crescut i cel al pacienilor care prezint titru crescut preoperator; *** Numrul pacienilor cu miastenie postoperatorie
raportat la numrul timoamelor cu miastenie; t intervalul de timp ntre rezecie i apariia miasteniei gravis

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Aceast form particular de miastenie


succede mai des forme invazive ale
timoamelor. Evoli i colab. [10] constat c
11 din cele 13 miastenii postoperatorii
(84,61%) au fost precedate de rezecia unor
tumori invazive [10]. De remarcat este faptul
c timoamele cu miastenie concomitent au
reprezentat 53,61% din leziunile invazive. O
remarc similar este fcut i Li i colab.
[14]: 8 din 15 cazuri de miastenie
postoperatorie (53,33%) au aprut dup
rezecia unor timoame n stadiul II i III.
Kondo numr 6 din 8 miastenii
postoperatorii ca fiind consecutive unor
timoame n stadiile II-IV [3].
Intervalul de timp scurs ntre apariia
miasteniei i momentul rezeciei timomului
este variabil (Tabelul I): de la perioada
postoperatorie imediat [13,14] pn la
cteva luni sau civa ani [6,9,10]. Intervalul
cel mai mare de timp n care au aprut
fenomenele bolii autoimune este de 18 ani
de la rezecia timomului. Sunt citate dou
astfel de cazuri unul cu [15] i altul fr
recidiv tumoral [7].
Din punctul de vedere al latenei
fenomenelor autoimune, lund ca reper 6
luni scurse de la intervenie, Ito mparte
miasteniile post-timectomie n miastenii
precoce i tardive [13].
Similar celorlalte forme de miastenie
(miastenia cu s-au fr timom), mecanismul
apariiei bolii la aceti pacieni nu este
cunoscut. Kuwata identific trei ipoteze
diferite: 1) recidiva sau metastazarea
timomului, 2) exereza unor timoame cu
forme infraclinice de miastenie i 3)
activarea postoperatorie a limfocitelor
periferice [16].
Miastenia gravis a fost citat ca factor
ce a evideniat recurena sau metastazarea
unor timoame non miastenice rezecate
[9,13,17]. Ito i colab. [13] remarc faptul c
multe din miasteniile aa zis tardive au fost
legate de recurena tumoral: 5 din 11
miastenii tardive au avut recderi tumorale
fapt nentlnit la cele 7 miastenii precoce.
Evoli, studiind 207 timoame cu miastenie
gsete 13 cazuri de miastenii postoperatorii
aprute [10]. Dintre acestea doar 3 (23%) au

fost asociate cu recurena tumoral [10].


Valori similare (20%) sunt raportate i n
studiul lui Nakajima i colab. [9]. Nici
exereza unei recurene a timomului nu
exclude apariia miasteniei postoperatorii.
Astfel, Tseng prezint un pacient care la 35
de luni dup rezecia unui timom B1 i
stadiul II Masaoka, este operat pentru o
metastaz pleural dreapt [18]. Dup alte
30 de luni dezvolt fenomenele miasteniei
gravis acesta fiind controlat prin tratament
cu cortizon i anticolinesterazice [18].
Ito i colab. [13] consider c
miasteniile dezvoltate n primele 6 luni sunt
expresia unor forme infraclinice de boal,
nedepistate la momentul rezeciei tumorale.
Din cele 15 miastenii prezentate de Li, 4 sau manifestat imediat dup terminarea
interveniei chirurgicale, autorul atrgnd
atenia asupra rolului favorizant al
medicaiei curarizante folosite intraoperator
[14]. Frecvena asocierii acestei evoluii
postoperatorii imediate: 4 din cele 127 de
timoame fr miastenie (3,14%), nu are
valori suficient de mari pentru a contraindica
de principiu utilizarea curarizantelor n
timpul rezeciei timoamelor. Un alt factor
incriminat n activarea acestor miastenii
infraclinice ar fi aminogliocozidele folosite
deseori n perioada postoperatorie [12].
n sprijinul mecanismului extra timic
de producie a autoanticorpilor, majoritatea
autorilor invoc dou studii. A fost
demonstrat faptul c celulele T existente n
timoame trec n sngele periferic, unde pot
persista pentru muli ani [19]. Prin
persistena acestor celule s-ar crea condiiile
secreiei extra timice a autoanticorpilor.
Acest mecanism este susinut i de
evidenierea eliberrii de ctre timoame n
torentul sangvin de mature auto-antigenspecific T-cells [20]. Triggerul declanrii
acestor fenomene autoimune rmne totui
necunoscut.
A fost observat o coresponden ntre
nivele
crescute
ale
autoanticorpilor
antireceptor de acetilcolin i riscul apariiei
miasteniei postoperatorii. Sun i colab. [12]
remarc faptul c 4 din cei 22 de pacieni
care au prezentat aceti
anticorpi

Miastenia gravis post timectomie

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Jurnalul de Chirurgie (Iai), 2013, Vol. 9, Nr. 2

preoperator, au dezvoltat mai trziu MG


(18,1%). Valori similare raporteaz i
Nakajima (23%) i Kondo (25%).
O importana perdictiv mai mare se
pare c o au autoanticorpii antifibr
muscular striat. n studiul lui Ohta i
colab. [11], din 46 de timoame fr
miastenie 18 au avut titruri crescute ale
acestor autoanticorpi preoperator i, din
acetia, 9 (50%) au dezvoltat miastenie. Mai
mult, din cei care au fost negativi la acest
test, niciunul nu a prezentat boala
postoperator [11].
Este cunoscut, dar totui controversat
nc, rolul timectomiei n tratamentul
miasteniei gravis. n cazul timoamelor,
Masaoka afirm c rezecia timusului i a
grsimii mediastinale asociate extirprii unui
timom micoreaz rata recidivelor i scade
riscul apariiei miasteniei postoperatorii [21].
Din pcate nu sunt prezentate i argumente
clinice cu privire la riscul miasteniei. Mai
mult, sunt numeroase studii care infirm
existena unei legturi dintre asocierea
rezeciei
timusului
i
a
grsimii
mediastinului anterior i riscul de apariie a
miasteniei postoperatorii. Observnd 18
miastenii postoperatorii din 394 de timoame
non-miastenice operate, Ito a calculat o rat
de apariie a miasteniei de 2,8% dup
timectomie i de 3,9% dup timo-timectomie
[13]. O observaie similar face i Nakajima
care constat c n 4 din cele 5 miastenii
postoperatorii s-a practicat timectomia
extins [9]. Mai mult din cele 8 cazuri
prezentate de Kondo, 2 au urmat dup o
timectomie extins i 6 dup timectomie [3].
Din cele 137 de cazuri n care s-a practicat
doar exereza tumorii niciunul nu s-a
complicat cu miastenie postoperatorie [3].
Dintr-un numr de 6 miastenii postoperatorii
studiate de Sun, 3 au aprut dup o
timectomie extins i 3 au sucedat o timotimectomie.
De observat c n niciun caz n care s-a
efectuat doar rezecia timomului nu s-a
constatat apariia misteniei postoperatorii
[12].

CONCLUZII
Remarcm faptul c, dei este o
entitate rar ntlnit n practic, miastenia
dup timectomie trebuie luat n considerare
n evoluia postoperatorie a pacienilor cu
timom. Dintre factorii predictivi ai acestei
boli sunt: invazivitatea tumorii, titrul
autoanticorpilor antifibr muscular striat i
cel al autoanticorpilor antireceptor de
acetilcolin. Asocierea timectomiei sau a
rezeciei
grsimii
mediastinale
nu
influeneaz riscul producerii acestei boli.
CONFLICT DE INTERESE
Autorii nu declar nici un conflict de
interese.

BIBLIOGRAFIE
1. Vincent A, Palace J, Hilton-Jones D.
Myasthenia gravis. Lancet. 2001; 357: 21222128.
2. Engels EA. Epidemiology of thymoma and
associated malignancies. Thorac Oncol. 2010;
5(10 Suppl 4): S260-S265.
3. Kondo K, Monden Y. Myasthenia gravis
appearing after thymectomy for thymoma. Eur
J Cardiothorac Surg. 2005; 28(1): 22-25.
4. Fershtand JB, Shaw RR. Malignant tumor of
the thymus gland, myasthenia gravis
developing after removal. Ann Intern Med.
1951; 34: 1025-1035.
5. Green RA, Booth CB. The development of
myasthenia gravis after removal of thymoma.
Am J Med. 1958; 25(2): 293-302.
6. Kang SY, Lee JS, Choi JC, Kang JH.
Myasthenia
gravis
appearing
after
thymectomy: a case report and review of the
literature. J Clin Neurol. 2007; 3(3): 158-160.
7. Shaulov A, Rottenstreich M, Peleg H, Spiegel
M, Shichman B, Argov Z.Myasthenia gravis
appearing 18 years after resection of benign
thymoma with subsequent limbic encephalitis.
J Neurol Sci. 2012; 317(1-2): 146-147.
8. Namba T, Grunner NG, Grob D. Myasthenia
gravis in patients with thymoma, with
particular reference to onset after thymectomy.
Medicine. 1978; 57: 411-433.
9. Nakajima J, Murakawa T, Fukami T, Sano A,
Takamoto S, Ohtsu H. Postthymectomy
myasthenia gravis: relationship with thymoma
and antiacetylcholine receptor antibody. Ann
Thorac Surg. 2008; 86(3): 941-945.

184

Mota C. et al.

Jurnalul de Chirurgie (Iai), 2013, Vol. 9, Nr. 2

10. Evoli A, Minisci C, Di Schino C, et al.


Thymoma in patients with MG: characteristics
and long-term outcome. Neurology. 2002;
59(12): 1844-1850.
11. Ohta M, Itoh M, Hara H, et al. Anti-skeletal
muscle and anti-acetylcholine receptor
antibodies in patients with thymoma without
myasthenia gravis: relation to the onset of
myasthenia gravis. Clin Chim Acta. 1991;
201(3): 201-205.
12. Sun XG, Wang YL, Liu YH, et al. Myasthenia
gravis appearing after thymectomy. J Clin
Neurosci. 2011; 18(1): 57-60
13. Ito M, Fujimura S, Monden Y, et al. A
retrospective group study on post-thymectomy
myasthenia gravis. Nihon Kyobu Geka Gakkai
Zasshi. 1992; 40(2): 189-193.
14. Li J, Zhang DC, Wang LJ, Zhang DW, Zhang
RG. Myasthenia gravis occurring after
resection of thymoma. Zhonghua Wai Ke Za
Zhi. 2004; 42: 540-542.
15. Shinkai T, Saijo N, Yoshioka S, et al.
Recurrence of thymoma with appearance of
myasthenia gravis 18 years after surgery. Jpn J
Clin Oncol. 1985; 15: 567-575.

16. Kuwata T, Iwata T, Iwanami T. Postthymectomy myasthenia gravis with an episode


of Osserman stage III. JSCR. 2012; 5: 3.
17. Denayer MA, Rao KR, Wirz D, McNally D.
Hepatic metastatic thymoma and myasthenia
gravis twenty-two years after the apparent cure
of an invasive thymoma. A case report and
review of the literature. J Neurol Sci. 1986;
76: 23-30.
18. Tseng YL, Chang JM, Shu IL, Wu MH.
Myasthenia gravis developed 30 months after
resection of recurrent thymoma. Eur J
Cardiothorac Surg. 2006; 29(2): 268-269.
19. Buckley C, Douek D, Newsom-Davis J,
Vincent A, Willcox N. Mature, long-lived
CD4+ and CD8+ T cells are generated by the
thymoma in myasthenia gravis. Ann Neurol.
2000; 50: 64-72.
20. Hoffacker V, Schultz A, Tiesinga JJ, et al.
Thymomas after the T-cell subset composition
in the blood: a potential mechanism for
thymoma associated autoimmune disease.
Blood. 2000; 96: 3872-3879.
21. Masaoka A. Staging system of thymoma. J
Thorac Oncol. 2010; 5(10 Suppl 4): S304S312.

CASE REPORT

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Jurnalul de Chirurgie (Iai), 2013, Vol. 9, Nr. 2

A CASE OF PENILE ENTRAPMENT IN METAL RINGS


TREATED BY ASPIRATION AND PUNCTURE TECHNIQUE
S. Kumar1 , A. Gupta2
1) Department of Surgery, Himalayan Institute Hospital Trust University, Dehradun, India
2) University College of Medical Sciences, Delhi, India
A CASE OF PENILE ENTRAPMENT IN METAL RINGS TREATED BY ASPIRATION
AND PUNCTURE TECHNIQUE (Abstract): INTRODUCTION: Application of constriction
over penis by means of various objects for autoerotic purpose is a practice that may lead to
dangerous consequences. A large variety of objects have been used for this purpose leading to a
spectrum of complications. Management of such cases poses a great challenge to the treating
surgeon, as it often requires teamwork involving not only doctors but also technical experts from
engineering department. We report a case where a man presented with acute retention of urine
with two metallic rings over his penis. CASE REPORT: A 50 years old man presented to the
surgical emergency ward with complaint of acute retention of urine. He had pushed two metallic
rings over his penis about two hours back in a bid to get sexual pleasure while he was under
influence of alcohol. The rings later got impacted over the penis because of congestion of distal
part of penis. Soon the patient developed the complaint of mild pain and swelling of penis and
inability to pass urine and was brought to the hospital. The physical exam revealed that the part of
penis distal to the rings was congested, swollen and slightly discolored. We started with urinary
bladder emptying by putting a wide bore needle suprapubically and connecting it to a urobag
through a drip set. Penile block was given. Blood was then aspirated from both corpora cavernosa
distal to the rings and the rings were manipulated after generous application of lubricant jelly.
This way, rings could be moved almost up to corona glandis obstructed only by a band of
edematous skin. Now multiple needle punctures were given in this skin and the area was kept
compressed for a while using a tape-gauze wrapped tightly over it. On removing the gauze, rings
could be moved up to corona. Now the distal ring was placed with its wide stone bearing part
against the ventral aspect of glans. Glans was then decongested by means of needle punctures and
digital compression. Ring was rotated with traction while glans was compressed to negotiate
through it. The attempt was successful and both rings were removed in this fashion. The post
operative course was uneventful. CONCLUSIONS: Aspiration and puncture technique facilitates
the removal of constricting objects from the penis. This technique is safe and does not require
sophisticated equipment.
KEY WORDS: PENILE ENTRAPMENT; METAL RINGS; ASPIRATION AND PUNCTURE
TECHNIQUE
SHORT TITLE: Penile entrapment: aspiration technique
HOW TO CITE: Kumar S, Gupta A. A case of penile entrapment in metal rings treated by aspiration and puncture
technique. Jurnalul de chirurgie (Iai). 2013; 9(2): 185-188. DOI: 10.7438/1584-9341-9-2-11.

INTRODUCTION
Application of constriction over penis
by means of various objects for autoerotic
purpose is a practice that may lead to
dangerous consequences. A large variety of

objects have been used for this purpose


leading to a spectrum of complications.
Management of such cases poses a great
challenge to the treating surgeon, as it often
requires teamwork involving not only

Received date: 23.02.2013


Accepted date: 15.03.2013
Correspondance to: Saurabh Kumar, MS, Assistant Professor of Surgery
Department of Surgery, Himalayan Institute Hospital Trust (H.I.H.T.) University
Swami Ram Nagar
PO Doiwala, Dist. Dehradun 248140
Uttarakhand, India
Phone.: 0091 (0) 81 93 97 87 35
Fax: 0091 (0) 13 52 47 13 17
E-mail: drsaurabhkumar@yahoo.co.in

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doctors but also technical experts from


engineering department. The emergency
physicians should be well aware of the
appropriate line of management in such
cases in order to be able to coordinate the
teamwork. We report a case where a man
presented with acute retention of urine with
two metallic rings over his penis.
CASE REPORT
A 50 years old man presented to the
surgical emergency ward with complaint of
acute retention of urine. He had pushed two
metallic rings over his penis about two hours
back in a bid to get sexual pleasure while he
was under influence of alcohol. The rings
later got impacted over the penis because of
congestion of distal part of penis. Soon the
patient developed the complaint of mild pain
and swelling of penis and inability to pass
urine and was brought to the hospital.
On examination he was conscious and
talkative but a little apprehensive. His vital
parameters were within normal limits. His
urinary bladder was distended and palpable.
He had two ornamental rings impacted over
his penis (Fig. 1). The part of penis distal to
the rings was congested, swollen and slightly
discolored. Tenderness was minimal.
At first an intravenous line was
established and the patient was given 200
mg of ciprofloxacin intravenously and 75
mg of diclofenac-sodium intramuscularly.
As wire cutters were not immediately
available in the emergency ward, a plan to
attempt removal of intact rings was made
before wire cutters could be arranged. To
start with urinary bladder was evacuated by
putting a wide bore needle suprapubically
and connecting it to a urobag through a drip
set. Penis was then cleaned and antiseptic
solution was applied. Penile block was
given. Blood was then aspirated from both
corpora cavernosa distal to the rings and the
rings were manipulated after generous
application of lubricant jelly.
This way, rings could be moved
almost up to corona glandis obstructed only
by a band of edematous skin. Now multiple
needle punctures were given in this skin and

the area was kept compressed for a while


using a tape-gauze wrapped tightly over it.
On removing the gauze, rings could be
moved up to corona. Now the distal ring was
placed with its wide stone bearing part
against the ventral aspect of glans. Glans
was then decongested by means of needle
punctures and digital compression. Ring was
rotated with traction while glans was
compressed to negotiate through it. The
attempt was successful and both rings were
removed in this fashion.
The patient was kept in the hospital for
a few hours under observation during which
there was no significant bleeding from
puncture wounds and patient could pass
clear urine without any difficulty. He was
discharged from the hospital thereafter on
oral ciprofloxacin. The patient was later seen
in outpatients department one week later. He
had no complaints related to micturition or
sexual intercourse and his penis looked
healthy.

Fig. 1 Penile entrapment in metal rings

DISCUSSION
Penile entrapment in a constricting
object is a surgical emergency requiring
immediate attention because of the risk of
irreversible ischemic injury. A large variety
of objects has been implicated in cases of
penile strangulation injury such as rings,
nuts, bushes, bottleneck, pipes and loop
wrench etc. Such objects are placed over
penis deliberately either for autoerotic
purpose or secondary to psychiatric
disturbance. Some people use constricting

Penile entrapment: aspiration technique

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band over penis in a bid to overcome


impotence. In children the constricting
objects are usually non-metallic such as
rubber band, thread or hair. These are used
to prevent enuresis or incontinence or may
represent an innocent childish experiment.
When an encircling object is placed
over penis it impairs the venous and
lymphatic return of penis while the arterial
flow is maintained. This results in
congestion of distal part of the penis and, if
the object is not removed, it gets impacted.
Patient may present with edema or
ulceration of penile skin, loss of sensation,
retention of urine, urethral fistula or even
gangrene. Bhat et al. [1] classified the penile
strangulation injury into five grades
according to severity, with grade one
characterized by only edema of distal penis
without skin ulceration or urethral injury,
grade two having injury to skin, constriction
of corpus spongiosum, distal penile edema
and decreased penile sensation, grade three
having injury to skin and urethra and
decreased penile sensation but no urethral
fistula, grade four comprising complete
division of corpus spongiosum leading to
urethral fistula and constriction of corpus
cavernosum with loss of distal penile
sensation, and grade five representing
gangrene, necrosis or complete amputation
of distal penis.
Management issues in such cases are
relief from retention of urine, removal of
constricting object, prevention of sepsis and
prevention or treatment of complications. To
relieve the retention of urine urethral
catheterization is possible in many cases
but suprapubic cystostomy is often
required [2,3].
The most challenging job however is
the removal of the constricting object. The
object may be either cut apart or removed
intact, depending upon the type and size of
the object, duration of penile incarceration
and the availability of equipment. Nonmetallic thin objects are easy to remove but
objects like thread or hair may erode deep
inside the skin and may cause severe urethral
injury. Thin metallic rings, at times, can be

removed easily by means of metal cutters


but a variety of tools has been used for this
purpose when the constricting object is
composed of hard metal and is difficult to
cut. These include saw, cutting tongs, high
speed drills, hammer and chisel, and Dremel
Moto-Tool etc. [1,4,5]. When a drill is used
to cut the object, a lot of heat is produced
which can cause thermal injury to
underlying penile tissue. To prevent this,
continuous irrigation with copious amount of
ice water is required [1,5]. Such
sophisticated tools are not easily available in
emergency wards and this lack of adequate
resources often warrants an attempt at
manual removal of the constricting object.
The choices of methods for removing
the object intact include the String Method
which was originally described by Flatt for
removing strangulating ring from a finger
[6]. Vahasarja et al. [7] reported two cases
successfully managed by this method.
Detweiler and Perkins [8] used latex band in
a similar fashion calling it the Wrapping
Technique. We used the Aspiration
Technique in this patient. Aspiration of
blood was done from the shaft and glans of
penis to achieve detumescence followed by
manual expression of fluid and successful
removal of the constricting agent. The penile
skin edema was overcome by wrapping the
penis tightly in a tape-gauze and thus
providing sustained compression over a
length of penis. So this combination of
maneuvers made it possible to remove the
two rings intact without the use of
sophisticated tools, leading to the desired
result and an uneventful recovery. There
have been few previous case reports of
successful use of this technique [9-11].
Surgery in the form of degloving of
penis to reduce its effective diameter may be
required in some patients. Coverage with
skin graft or flap is required. Surgery is also
indicated in case there is ulceration or
necrosis of skin, debridement of devitalized
tissue is done followed by skin
replacement [3]. Urethra should be evaluated
radiologically soon after removal of the
constricting object if injury is contemplated.

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Urethral fistula may require reconstruction.


Urethral stricture may be a late
complication.
CONCLUSION
Aspiration and puncture technique
facilitates the removal of constricting objects
from the penis. This technique is safe and
does not require sophisticated equipment.
The procedure saves valuable time and
hence may prevent development of
irreversible ischemic changes in many cases.
In our case the technique was used
successfully with an uneventful recovery.
CONFLICT OF INTEREST
The author and co-author have no
conflict of interest.
REFERENCES
1. Bhat AL, Kumar A, Mathur SC, Gangwal KC.
Penile Strangulation. British J Urol. 1991; 68:
618-621.
2. Snoy FJ, Wagner SA, Woodside JR, Orgel
MG, Borden TA. Management of penile
incarceration. Urology. 1984; 24: 18-20.

3. Klein FA, Smith MJ. Treatment of


incarceration of the penis by tempered steel
bushings. J Emerg Med. 1987; 5(1): 5-8.
4. Kadioglu A, Cayan S, Ozacn F, Tellaloglu S.
Treatment of penile incarceration in an
impotent man. Int Urol Nephrol. 1995; 7: 639641.
5. Shuster G, Stockmal P. Genital incarceration
with metal rings; their safe removal.
Techniques in urology. 1999; 5: 116-118.
6. Flatt AF. The care of minor hand injuries. 2nd
ed. St. Louis: CV Mosby; 1963. p. 262-263.
7. Vahasarja VJ, Hellstrom PA, Serlo W,
Kontturi MJ. Treatment of penile incarceration
by the string method: two case reports. J Urol.
1993; 149: 372-373.
8. Detweiler MB. Penile incarceration with metal
objects: A review of procedure choice based
on penile trauma grade. Scand J Urol Nephrol.
2001; 35: 212-217.
9. Punekar SV, Shroff RR, Vaze ML. An unusual
case of strangulation of penis by metal
hammer head( a case report). J Postgrad Med.
1978; 24: 58-59.
10. Sinha BB. Penile incarceration by a metal ring.
Br J Surg. 1988; 75: 33.
11. Bermudez AMT. Incarceration del pene por
object metalico pesado. Arch Esp de Urol.
1998; 51: 483-484.

CASE REPORT

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GIANT SUBMUCOSAL GASTRIC LIPOMA CASE REPORT


Maria-Gabriela Aniei1 , I. Huanu1, A. Gervescu1, Oana Simionescu1,
Nora Lefter2, V. Scripcariu1
1) University of Medicine and Pharmacy Gr.T. Popa Iai, Romania
First Surgical Oncology Unit, Regional Institute of Oncology, Iai, Romania
2) Municipal Hospital, Gastroenterology Unit, Gura Humorului, Romania
GIANT SUBMUCOSAL GASTRIC LIPOMA CASE REPORT (Abstract): Gastric lipomas are
rare benign tumors, representing less than 1% of all gastric tumors. They often have a submucosal
origin, but in rare cases could originate in the subserosa. We report the case of a 72 year-old male
who presented dyspeptic syndrome and superior gastro-intestinal bleeding (melena). The upper
gastrointestinal endoscopy revealed a large, almost stenotic, submucosal oval-shaped mass, with a
diameter of 10 cm located in the gastric antrum, with an area of ulcerated gastric mucosa. The
abdominal computer tomography revealed a homogeneous well-defined mass with negative
densitometry values that corresponded to the fatty tissue. The tumor was enucleated through
antrotomy, with an uneventful postoperative course. CONCLUSION: Although rare, the gastric
lipoma can be a cause of gastrointestinal bleeding, mimicking a malignant tumor.
KEY WORDS: GASTRIC LIPOMA; GASTROTOMY; TUMOR ENUCLEATION
SHORT TITLE: Gastric lipoma
HOW TO CITE: Aniei MG Huanu I, Gervescu A, Simionescu O, Lefter N, Scripcariu V. Giant submucosal gastric
lipoma case report. Jurnalul de chirurgie (Iai). 2013; 9(2): 189-192. DOI: 10.7438/1584-9341-9-2-12.

INTRODUCTION
Gastrointestinal lipomas are rare
benign tumors that may occur anywhere
along the gut. Most of them are located in
the colon, ileum and jejunum [1,2]. With
only 220 cases reported in the literature [14], gastric lipomas are even more unusual,
and they occur mostly in the antrum having
a submucosal origin [5]. The imaging
examination can be highly suggestive for the
diagnosis, while the histological examination
offers the final and certain diagnosis.
Computed Tomography (CT scan) is the
imaging examination of choice for obtaining
a specific diagnosis of lipoma [6]. However,
the tumor may sometimes undergo
significant inflammatory changes leading to
a difficult differential diagnostic with the
well-differentiated liposarcoma.

CASE REPORT
We examined a 72 years old man with
a 4 month history of dyspeptic disorder,
fatigue and melena, and without significant
weight loss. He was previously medically
treated with i.v. fluids and haemostatics. The
medical history was significant for
hypertension, atrial fibrillation and heart
failure stage II NYHA. The administered
medication included warfarin, diuretics,
clopidogrel, angiotesin II receptor blocker,
calcium channels blockers and selective
beta-blocker.
Physical examination reveals an obese
patient (BMI=30.5 kg/m2), with a general
good status, and slightly pale teguments. The
abdomen was flat and soft, with mild
tenderness in epigastrum and no palpable
masses.

Received date: 28.02.2013


Accepted date: 25.03.2013
Correspondance to: Maria-Gabriela Aniei, MD
First Surgical Oncology Unit, Regional Institute of Oncology Iai
Str. General Henri Mathias Berthelot no 2-4, 700483 Iai, Romania
Phone: 0040 (0) 374 27 88 10
Fax: 0040 (0) 374 27 88 02
E-mail: dr.mgabriela@gmail.com

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Laboratory tests showed anemic


syndrome
(hemoglobin
8.8
mg/dL,
hematocrit 28.5%); tumor markers showed
no abnormalities (CEA and CA19-9 in
normal range). Blood chemistry profile and
coagulation samples were within normal
limits.
The upper gastrointestinal endoscopy
revealed a large, oval-shaped, submucosal
stenosing tumor, located in the gastric
antrum. An area of ulceration was identified
in the center of the tumor. Many biopsies
were obtained (from superficial and deep
layers), but they only showed unspecific
inflammation of the gastric mucosa.
The CT scan revealed a homogeneous
oval-shaped, well defined soft tissue mass in
the gastric antrum area, measuring
approximately 5.3 x 8.1 x 6.2 cm, with
negative densitometry values (-70 and -120

Hounsfield units) that correspond to fatty


tissue (Fig. 1), which on the barium study
appeared as a smooth filling defect with a
bulls eye appearance, slightly pressing on
the duodenum.
The tumor was suspected to be a
lipoma, a leiomyoma or a leiomyosarcoma.
The patient underwent midline
supraumbilical laparotomy. The antropyloric region of the stomach reveals a
yellowish, well defined tumor, with a
longitudinal diameter of 8.5 cm, placed in
the posterior wall of gastric antrum, at a
distance from the pyloric canal, without any
other pathological findings.
The tumor was totally removed
through an incision of gastric serosa and
subserosa, dissected from the gastric mucosa
and enucleated (Fig. 2).

Fig. 1 CT-scan image showing a well-defined oval


mass on the gastric antrum

Fig. 2 Intraoperative view showing a yellowish


subserosal neoplasm on the posterior wall of gastric
antrum (up and middle) and the adhesion area of the
gastric mucosa (bottom)

An edge resection of the underlying


layers, with endoluminal check of the gastric
mucosa was performed, due to a 1 cm2 area
of adhesion of the tumor to the gastric
mucosa (Fig. 2, bottom).

The gastrostomy was closed with PDO


3.0 in a single layer and epiploonoplasty was
performed.
The pathological exam revealed that
the mass is a submucosal lipoma, measuring

Gastric lipoma

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11 x 6.5 x 4 cm diameter, with areas of


mucosal ulceration.
The patient underwent an uneventfull
recovery and he was discharged on the
seventh postoperative day.
DISCUSSIONS
Most of the gastro-intestinal lipomas
can be found along the colon, ileum and
jejunum. Lipomas of the esophagus and
stomach represent approximately 5% of all
gastrointestinal lipomas, and when they are
located in the stomach, the predilection site
is the antrum. Small lipomas are usually
asymptomatic, while 75% of those bigger
than 4 cm can generate symptoms, most
frequently gastrointestinal bleeding in 50%
of the patients [7], anemia, abdominal pain,
dyspeptic syndrome and even obstruction
[8]. In the present case, the patient presented
upper
gastrointestinal
hemorrhage
manifested by melena, dyspepsia, all due to
the large size of the tumor.
To
the
upper
gastrointestinal
endoscopy, gastric lipomas appear as soft,
very well defined, submucosal masses.
There are 3 clues helping to identify these
tumors as lipomas on endoscopy: the tenting
sign (the overlying mucosa is easily
retracted with the biopsy forceps), the
cushion sign (the forceps produces a soft
indentation on the surface of the lipoma) and
naked fat sign, when fat protrudes through
the overlying mucosa after multiple biopsies
[9,10]. In the current case, the endoscopy
identified the mass in the gastric antrum, but
the tree signs were not present, probably due
to the size of the tumor; the lesion may be
associated with a central superficial
ulceration [5]. The endoscopic ultrasound
can be used to diagnose gastric lipomas [11]
and it can identify the originating layer, the
depth and the size of the tumor [12], but in
our case it was not performed, for logistic
reasons.
High resolution ultrasound has a
detection rate of 93% in identifying
submucosal masses [13]. It is difficult to do
a histopatologic diagnostic after the
endoscopic biopsy of these tumors, mainly

because the tumors are submucosal and the


obtained sample contains nonspecific tissue,
such as inflammatory tissue. CT scan
appears to be the most reliable diagnostic
tool for ulcerative gastric lipoma [6] and this
was the examination that suggested the
diagnosis, due to the specific densitometry
of the fatty tissue.
Lipomas are benign tumors and
extensive gastric resections are not the
choice in these cases [1]. The simple
enucleation of the tumor or partial gastric
resection have to be applied. Endoscopic
polipectomy for tumors smaller than 3 cm
gained consensus on safety and efficacy [9],
while laparoscopic removal of large gastric
lipomas has been successfully performed
and offers advantage over an open surgery.
The therapeutic choice in this case was
suggested by the imagistic diagnostic tools,
especially CT-exam, but also by the
intraoperative findings. The ulcerated area of
the lipoma can explain the bleeding, but it
can also be the consequence of the multiple
biopsies. The certainty of the diagnostic was
offered
by
the
histopathological
examination.
CONCLUSIONS
Gastric lipomas, depending on the size
and
topography,
can
induce
a
symptomatology mimicking more aggressive
upper gastrointestinal tract pathology.
In most cases, lipomas are not taken
into consideration as a possible differential
diagnosis for the malignant tumors.
Imagistic exams can be highly suggestive for
a submucosal, benign tumor, while the
histopathological examination of the whole
resected specimen gives the final diagnosis,
the endoscopic biopsies being often
inconclusive.
In our case, the CT-scan suggested the
diagnostic and the applied surgical treatment
was the simple enucleation of the tumor.

CONFLICT OF INTEREST
The authors have no conflict of
interest.

Aniei MG. et al.

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1.

2.

3.

4.

5.

6.

REFERENCES
Salzman JR, Carr-Locke DL, Fink SA.
Lipoma case report. Med Gen Med. 2005;
7(1): 16.
Trcoveanu E, Cotea E, Nicolescu S, et al.
[Clinical significance and management in
colonic lipomas]. Jurnalul de chirurgie (Iai).
2007; 3(4): 370-377.
Treska V, Pesek M, Kreuzberg B, Chudacek
Z, Ludvikova M, Topolocan O. Gastric lipoma
presenting
as
upper
gastrointestinal
obstruction. J Gastroenterol. 1998; 33(5): 716719.
Antes G, Neher M. Lipoma of the stomach
diagnosis and therapy. Rontgenpraxis. 1995;
48(9): 252-253.
Hamdane MM, Brahim B, Belhaj Salah M,
Haouas N, Bouhafa A, Chedly-Debbiche A.
Giant gastric lipoma mimiking welldifferentiated liposarcoma. Gastroenterol
Hepatol Bed Bench. 2012; 5(1): 60-63.
Thompson WM, Kende AI, Levy AD. Imaging
characteristics of gastric lipomas in 16 adult
and pediatric patients. Am J Roentgenol. 2003;
181(4): 981-985.

7. Ciraldo A, Thomas D, Schmidt S. Gastric


lipoma presenting as gastrointetsinal bleeding :
a case report. The Internet Journal of
Advanced Nursing Practice. 2000; 1(1): DOI:
10.5580/1392.
8. Zameer M, Kanojia RP, Rao KLN, Menon P,
Samujn R, Thapa BR. Gastric lipoma. J Indian
Assoc Pediatr Surg. 2010; 15(2): 64-66.
9. Taylor AJ, Stewart ET, Dodds WJ.
Gastrointestinal lipomas: a radiological and
pathologic view. Am J Roentgenol. 1990;
55(6): 1205-1210.
10. DeBeer RA, Shinye H. Colonic lipomas. An
endoscopic analysis. Gastrointest Endosc.
1975; 22(2): 90-91.
11. Chak A. EUS in submucosal tumors. Gastrointest
Endosc. 2002; 56 (4 supll): S43-S48.
12. Krasniqi AS, Hoxha FT, Bicaj BX, et al.
Symptomatic subserosal gastric lipoma
successfully treated with enucleation. World J
Gastroenterol. 2008; 14(38): 5930-5932.
13. Tsai TL, Changchien CS, Hu TH, Hsiaw CM.
Demonstration of gastric submucosal lesions
by high resolution transabdominal sonography.
J Clin Ultrasound. 2000; 28(3): 125-132.

SURGICAL TECHNIQUE & MULTIMEDIA

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LAPAROSCOPIC TRANSABDOMINAL PRE-PERITONEAL


(TAPP) PROCEDURE FOR GROIN HERNIA.
HOW TO DO IT FOR BETTER OUTCOMES
R. Moldovanu
1) Department of surgery, University of Medicine and Pharmacy Gr.T. Popa Iai, Romania
2) Department of surgery and oncology, Les Bonnettes Hospital, Arras, France
LAPAROSCOPIC TRANSABDOMINAL PRE-PERITONEAL PROCEDURE (TAPP) FOR
GROIN HERNIA. HOW TO DO IT FOR BETTER OUTCOMES (Abstract): The laparoscopic
approach for the groin hernia repair has several advantages: decreased immediate and late
postoperative pain, less numbness in inguinal aria, less mesh infection and a rapid recovery.
However the good outcomes are not granted, and there are some key points to be followed for
better postoperative results. The aim of this video is to highlight these TAPP (TransAbdominal
Pre-Peritoneal) related key points, from the operative indication, pre operative preparation and
surgical procedure, until the post operative follow up.
KEY WORDS: LAPAROSCOPY;
PERITONEAL PROCEDURE (TAPP)

GROIN

HERNIA;

TRANSABDOMINAL

PRE-

SHORT TITLE: TAPP How to do it


HOW TO CITE: Moldovanu R. Laparoscopic transabdominal pre-peritoneal procedure (TAPP) for groin hernia. How to
do it for better outcomes. Jurnalul de chirurgie (Iai). 2013; 9(2): 193-196. DOI: 10.7438/1584-9341-9-2-13.

Video
BACKGROUND
The laparoscopic approach for the
groin hernia repair has several advantages:
decreased immediate and late postoperative
pain, less numbness in inguinal aria, less
mesh infection and a rapid recovery [1].
However the good outcomes are not granted,
and there are some key points to be followed
for better postoperative results.
The aim of this video is to highlight
these
TAPP
(TransAbdominal
PrePeritoneal) related key points, from the
operative
indication,
pre
operative
preparation and surgical procedure, until the
post operative follow up.
TAPP INDICATIONS:
TAPP can be performed in any type of
hernia, even in complicated (strangulated)

hernia [2,3]. Relative contraindications are


the large inguino-scrotal hernias and history
of radical prostatectomy [2,3]. Different
general comorbidites (e.g. heart failure,
chronic
respiratory
disease)
can
contraindicate the general anesthesia and, as
consequence, the TAPP [2,3].
PREOPERATIVE PREPARATION
There is no particular preparation;
however it has to be highlighted the
importance of comorbidites evaluation and
adequate skin preparation. In this way it is
important to note the preoperative antiseptic
shower, the hair removing using a barber
clipper, use of alcoholic based solution for
skin preparation and the bladder emptying
just before the procedure (facilitate the
dissection and avoid bladder injuries) [2-4].

Received date: 28.02.2013


Accepted date: 12.03.2013
Correspondance to: Radu Moldovanu, MD, PhD
Departament of Surgery and Oncology, Les Bonnettes Hospital, Arras, France
2 rue Dr. Forgeois, 62012, Arras, Cedex, France
Phone: 0033(0) 3 21 60 22 70
Fax: 0033(0) 3 21 60 22 58
E-mail: rmoldovanu@gmail.com

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ANESTHESIA AND OPERATIVE


ROOM SET-UP; INSTRUMENTS
General anesthesia is mandatory. The
patient is placed in supine position, in a 15
Trendelenburg tilt with both arms in
adduction along the body; the laparoscopic
tower is placed to the feet of the patient as
the display to be located on the hernias site
[5,6]. The surgeon operates from the
opposite side of the hernia near the patients
shoulder, and the assistant stands opposite to
the surgeon [5,6].
Three trocars are used: one of 10 mm
and two of 5 mm. Common laparoscopic
instruments (fenestrated graspers, scissors,
hook, needle holder etc.) are necessary. The
30 laparoscope is preferable [5].
SURGICAL PROCEDURE:
Usually the pneumoperitoneum is
performed using a Veress needle [5]. The
open technique is used in patients with
previous abdominal surgery and/or umbilical
hernia. The 5 mm trocars are inserted under
laparoscopic view control, laterally from the
epigastric vessels to improve the ergonomics
and triangulation [5].
The procedure starts by a careful
exploration of the abdomen identifying the
superficial anatomical landmarks (urachus,
umbilical folds, epigastric vessels, spermatic
vessels, vas deferens or uterine round
ligament) and the site and type of hernia [7].
Then a large opening of the
peritoneum is performed, from the anterosuperior iliac spine until the lateral umbilical
ligament (umbilical artery cord) 2 to 3 cm
beyond the parietal defect [1,3-6,8].
The dissection starts in Retzius space,
in contact with abdominal rectus muscles, from
laterally to medial and from cranial to
caudal, targeting the pubic bone, dividing
the fine conjunctive fibers (angel hair)
[1,5]. Then, the dissection is conducted from
medial to lateral into the Bogros space, from
epigastric vessels to spermatic vessels [5]. In
the same time we start the dissection of
hernia sac. The hernia sac is completely
dissected using traction contra-traction
maneuvers, sharp and blunt dissection and

fine coagulation; it is mandatory to find the


avascular plan to preserve the spermatic
fascia and to protect the fragile parietal
structures (vas deferens, vessels and nerves)
[1,5,8]. The dissection has to be conducted
in obturator fossa to identify the
occult obturator hernias (type I obturator
hernia) [5]. The dissection is completed
when all the deep anatomic landmarks
(Cooper, Gimbernat ligaments, corona
mortis and external iliac vein) are well
exposed and the pre peritoneal space is wide
opened (at least 12 x 15 cm) to allow the
correct mesh deployment and parietalization
[1,5,8].
It is important to search, dissect and
remove the cord or pre peritoneal lipoma,
because the overlooked lipomas could
be misdiagnosed as recurrent hernia or
seroma [9].
Afterwards, a large (12 x 15 cm) light
weight mesh is deployed in pre peritoneal
space, positioning to cover all the parietal
defects and fixed in appropriate position
using absorbable staples [1-3,6,8]. For
the bilateral hernia two overlapping mesh
are used, stapled together on the
midline [1-3,6,8].
In case of large hernia or after difficult
dissection or in patients with risk of
hemorrhage a suction drain is inserted in
Retzius space [10]; it will be removed after
12 to 24 hours postoperatively.
The peritoneum is then carefully
closed using continuous non absorbable
suture secured with an extracorporeal knot;
the closure using staples or barbed sutures is
also possible [5]. The closure has to be
waterproof to avoid small bowel
herniation [2,3].
The trocars are then removed under
laparoscopic control view. Usually the trocar
sites are infiltrated using ropivacaine, under
laparoscopic view [5]. The pneumoperitoneum is then exsufflated and the
trocars wounds are closed [5].
POSTOPERATIVE PERIOD
The usual postoperative analgesic
therapy consists in anti inflammatory non

TAPP How to do it

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Jurnalul de Chirurgie (Iai), 2013, Vol. 9, Nr. 2

steroid drugs (Paracetamol and Ketoprofen).


Usually the patients are discharged in the
same day or in first postoperative day [5]. To
further control the pain, all the patients
received a prescription with Paracetamol 500
mg x 3/day and Ketoprofen 100 mg x 2/day
for the first 7 days [5]. A routine thromboembolic disease prophylaxis with lightweight heparin therapy for 7 days for all the
patients, is usually performed even the
subject is controversy [2,3,5].
COMPLICATIONS
Different postoperative complications
are noted in the literature: seroma,
hematoma, chronic pain, ischemic orchitis or
testicular atrophy, infertility.
Seroma is the most frequent
complication of TAPP repair [2,3]; in my
experience, I noted a 6% rate, [11] close to
the rate reported in literature (5.7%) [2,3];
furthermore I noted a decreasing rate of
seroma after the use of suction drains.
Hematoma is less frequent in
endoscopic hernia repair than in open
repairs, with a rate of about 8% [2,3]; in my
experience, hematoma was noted in only
1.8% cases [11].
Chronic pain, defined as persistence of
pain 3 months after the operation [12], is less
frequent in endocopic techniques, and
especially after TAPP, than in open hernia
repair [2,3]; it was noted in 0.6% in a
previous work [11].
Several other complications after
TAPP were reported in the literature with an
incidence rate of 1% or less: wound / mesh
infection, urinary retention, bladder damage,
mesh migration, bowel obstruction, ischemic
orchitis / testicular atrophy [2,3].
The recurrence rate varies between 0.4
to 4.8% [2,3,13]; I noted a 0.6% rate of
recurrence and open anterior approach
(Lichtenstein repair) has performed [11].
CONCLUSIONS
TAPP is valuable procedure for the
cure of groin hernia; is associated with low
rate of postoperative morbidity and
recurrence. Both superficial and deep

anatomic landmarks are easily recognizable.


The laparoscopic exploration allows the
treatment of incarcerated / strangulated
hernias and the intra operative diagnosis of
occult hernias. The procedure is suitable for
day surgery.
CONFLICT OF INTERESTS
None to declare
REFERENCES
1. Collaboration EH. Laparoscopic compared
with open methods of groin hernia repair:
systematic review of randomized controlled
trials. Br J Surg. 2000; 87(7): 860-867.
2. Simons MP, Aufenacker T, Bay-Nielsen M, et
al. European Hernia Society guidelines on the
treatment of inguinal hernia in adult patients.
Hernia. 2009; 13(4): 343-403.
3. Bittner R, Arregui ME, Bisgaard T, et al.
Guidelines for laparoscopic (TAPP) and
endoscopic (TEP) treatment of inguinal Hernia
[International Endohernia Society (IEHS)]
Surg Endosc. 2011; 25: 2773-2843.
4. Tanner J, Moncaster K, Woodings D.
Preoperative hair removal: a systematic
review. J Perioper Pract. 2007; 17: 118121,
124132.
5. Moldovanu R, Pavy G. Laparoscopic
transabdominal pre-peritoneal (TAPP) for
bilateral inguinal hernia. Jurnalul de chirurgie
(Iai). 2010; 6(3): 373-382.
6. Leroy J. Transabdominal preperitoneal
approach
(TAPP).
E-publication:
WeBSurg.com,
Mar
2001;
1(3).
[available online at http://www.websurg.com
/ref/doi-ot02en194.htm]
7. Trcoveanu E, Bradea C, Moldovanu R.
Anatomia laparoscopic a regiunii inghinale.
Jurnalul de chirurgie (Iai); 2006; 1(4): 436446.
8. Bittner R, Leibl BJ, Jager C, Kraft B, Ulrich
M, Schwarz J. TAPP - Stuttgart technique and
result of a large single center series. Journal of
Minimally Access Surgery. 2006; 2(3): 155159.
9. Nasr AO, Tormey S, Walsh TN. Lipoma of the
cord and round ligament: an overlooked
diagnosis? Hernia. 2005; 9: 245-247.
10. Tamme C, Scheidbach H, Hampe C, Schneider
C, Kockerling F. Totally extraperitoneal
endoscopic inguinal hernia repair. Results of
5203 hernia repairs. Surg Endosc. 2003; 17:
192195.
11. Moldovanu R, Pavy G. Transabdominal
preperitoneal (TAPP) laparoscopic inguinal
hernia operation a learning curve analysis.
Chirurgia. 2012; 107(Suppl 1): S373.

196

Moldovanu R.

Jurnalul de Chirurgie (Iai), 2013, Vol. 9, Nr. 2

12. Aasvang E, Kehlet H. Classification of chronic


pain. Descriptions of chronic pain syndromes
and definitions of pain terms. Prepared by the
International Association for the Study of
Pain, Subcommittee on Taxonomy. Pain.
1986; Suppl 3: S1S226.

13. Bittner R, Schmedt CG, Schwarz J, Kraft K,


Leibl BJ. Laparoscopic transperitoneal
procedure for routine repair of groin
hernia. Br J Surg. 2002; 89(8): 1062-1066.

ARC PESTE TIMP

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Jurnalul de Chirurgie (Iai), 2013, Vol. 9, Nr. 2

CONTRIBUTION LA TECHNIQUE DU PNEUMOTHORAX


EXTRA-PLEURAL - 75 CAS OPRS
Cornel Crpinian et Mircea Oncesco
Sanatorium T.B.C. Moroieni, directeur Dr. C. Bibicesco
Revista de Chirurgie 1940; 9-10/43: 671-679.
Le
pneumothorax
extra-pleural
consiste en un acte opratoire de
dcollement pleuro-parital, apical et
mediastinal, qui permet de collaber les
lsions pulmonaire avec un quilibre optime
des tensions lastiques du poumon, et de
maintenir ce collapsus quilibr par des
insufflations ultrieures.
Cette mthode, pratique pour la
premire fois, et abandonne ensuite, en
1891 par Tuffier, a t reprise par Mayer,
Jensen
et
Nissen,
avec
certaines
modifications, pour tre tudie enfin en ces
derniers temps, en ce qui concerne les
indications ainsi que la technique, par lcole
allemande conduite par Graf et Schmidt, et
ensuite par Maurer, Hautefeuille, Brard etc.
A la suite de leurs travaux, la mthode
sest gnralise, tant pratique dans tous
les centres de tuberculose.
Chez nous, en Roumanie, elle a t
applique pour la premire fois en juin 1937
par lun de nous deux, le dr. Cornel
Crpinian avec dexcellents rsultats.
Dans cet article nous nallons pas
aborder les indications du pneumothorax
extra-pleural,
qui
appartiennent
exclusivement au domaine du phtisiologue,
mais nous nous bornerons dcrire la
technique opratoire avec les modifications
que nous lui avons apportes, les
complications et les rsultats obtenus.
Lopration est faite sous anesthsie
loco-rgionale, prcde dune injection de
Dilaudid-Atropine ou Scopolamine Knoll et
0,01 gr Morphine.
Nous faisons le blocage des nerfs
intercostaux dans langle costo-vertbral

avec Salvocane Salvator 0,75%, sans


dpasser la quantit de 100 -120 cm.
Schmidt indique la voie daccs par
lespace inter-scapulo-vertbral, par une
incision oblique allant de haut en bas et du
dedans en dehors, longue de 10-12 cm et
parallle au bord intrieur de lomoplate,
ayant le centre situ sur la 3-me ou 4-me
cte, ou bien par une incision transversale
dans le prolongement de lpine de
lomoplate.
La section du bord externe du muscle
trapze et la dissociation des fibres du
muscle rhombode, suivies dune rsection
sous-priostale de la 3-me ou 4-me cte,
avec la rsection du paquet vasculo-nerveux
respectif pour viter les hmorragies
loccasion des ponctions ultrieures, et afin
de crer une zone danesthsie en vue du
mme but. Schmidt indique comme point de
repre, pour trouver le plan de clivage, le
nerf intercostal.
Le dcollement se fait avec le doigt ou
laide de la pince munie de tampon, sous le
contrle de lil, sous la lumire de la sonde
de Schmidt, dans le plan de clivage de la
fascia endo-thoracique, qui consiste, comme
entit anatomique, en un tissu cellulaire laxe
extrapleural.
Pour avoir une bonne cavit
extrapleurale, il est absolument ncessaire
que le dcollement intresse tout le sommet
du poumon jusquau hile, les 6-7 ctes
postrieures et les 3-4 antrieures.
Aprs le contrle, on ferme
hermtiquement la cavit pleurale, plan par
plan.
De cette manire on russit crer une
cavit recouverte de tissu conjonctive solide,

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Jurnalul de Chirurgie (Iai), 2013, Vol. 9, Nr. 2

en exceptant la partie mdiastinale, cavit


elastique qui se maintient delle mme sans
ncessiter de grandes suprapressions
Schmidt.
Les modifications techniques que
nous venons dintroduire:
Il arrive bien rarement quune
opration type soit excute exactement
selon la description ou la manire
pratique par son promoteur, mais presque
toujours le chirurgien doit ladapter la
lsion. Ce qui intresse en dernire analyse,
cest le rsultat, mais il y a certaines
modifications dordre esthtique, pratique et
thrapeutique quil faut bien considrer.
Conduits par ce principe, nous avons
quitt la voie daccs indique par Graf et
Schmidt et nous avons abouti pntrer dans
lespace extrapleural, au niveau de la 7-me
ou 8-me cte, paralllement celle-ci et
perpendiculairement sur la ligne axillaire
postrieure, par une incision qui ne dpasse
pas la longueur de 5-6 cm.
On fait la rsection sous-priostale de
la cte, sur une tendue de 5 cm. On ne
rsque pas le paquet vasculo-nerveux, et on
pntre dans lespace extrapleural par
lincision du prioste qui reste sur place.
A laide dune sonde cannele
recourbe, nous pntrons dans lespace
dcollable et ensuite, nous faisons le
dcollement avec des tampons monts sur 2
pinces courbes, longues de 30 cm.
Toute cette manoeuvre est faite sous le
contrle de loeil, laide dune sonde
lumineuse et strilisable de Schmidt.
Le dcollement est la partie essentielle
de cette opration; cest lui donc quil faut
fixer toute notre attention.
Aprs le dcollement fait avec le doigt
tout autour de la plaie, nous continuons avec
une pince longue de 30 cm, au bout de
laquelle est mont un gros tampon
triangulaire de gaze. Nous agrandissons le
dcollement avec cette pince, en glissant la
paroi costale, en pressant le poumon au
niveau de langle de clivage.
Lorsque la cavit est suffisamment
agrandie pour pouvoir lclairer avec la

sonde lumineuse de Schmidt, nous


introduisons aussi la deuxime pince longue
avec des tampons. Nous continuons le
clivage de cette manire: pendant que laide
nous carte les lvres de la plaie avec deux
carteurs Farabeuf et un autre tient la sonde
lumineuse dans la cavit, nous dcollons en
pressant le poumon avec la pince de la main
gauche et de la droite nous continuons le
clivage.
Donc, notre conduite sans tre une
rgle, est la suivante: nous dcollons la
partie antrieure jusquau niveau du sternum
et en haut, jusquau sommet et aprs, la
partie postrieure jusqu langle costovertbral; nous dcollons la plvre paritale
du mdiastin postrieur, et aprs nous
librons le poumon du mdiastin antrieur et
la fin nous pressons de la pince de la main
gauche, le sommet du poumon et de la
droite, nous dcollons langle supro-interne
jusquau hile.
La libration du sommet pulmonaire se
fait beaucoup plus facilement si nous lavons
dcoll au pralable du mdiastin antrieur
et postrieur. Le dcollement du mdiastin
postrieur produit, presque dans tous les cas,
une toux rebelle qui ne peut tre prvenue
avec aucun opiac et qui, mme si elle est un
peu fcheuse pour loprateur, est bonne
pour le malade qui expectore le contenu des
bronches provenu de la collabation de la
partie malade, empchant ainsi, jusqu un
certain point, laspiration dans la partie
oppose(Schmidt).
Nos
dcollement
touchent en bas, postrieurement, les 9-10mes ctes et antrieurement les 5-6-mes et
mme la 7-me.
Dans certains cas [] le dcollement a
t fait aussi du diaphragme- aprs une
pralable phrnicectomie et de cette
manire, nous avons largi les indications
du pneumothorax extra-pleural aux cavernes
du lobe infrieur et mme jusquaux
cavernes de la base qui peuvent aussi
bnficier des avantages de la mthode.
Aprs le contrle de la cavit cre et
avant de la fermer, nous badigeonnons toute
la surface avec une solution de Clauden 2
fioles.

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Schmidt recommande le badigeonnage


au srum physiologique trs chaud.
Nous faisons la fermeture de la plaie
avec le prioste des ctes avoisinantes- la
moiti infrieure de la cte suprieure et la
moiti suprieure de la cte infrieure
(Hautefeuille). Suture du tissu cellulaire
sous-musculaire et des muscles dissocis et
du tissu cellulaire sous-cutan. Les
tguments nous les runissons par 6-8
agraffes Michel.
Graf maintient un drainage provisoire
de la cavit pendant quelques jours, pour
quilibrer la pression intra-cavitaire, parce
que le pneumothorax intrapleural assure le
collapsus en tapes, tandis que le
pneumothorax extrapleural chirurgical le
produit dun coup.
Lopration est peu choquante et
assure le collapsus de toutes les parties, en
maintenant en mme temps la fonction
expectorante (Hautefeuille).
Pour que la pneumolyse soit lective,
il faut quelle dpasse toujours la zone
pulmonaire malade et cest surtout pour cette
raison que nous dpassons de beaucoup cette
zone, pour avoir un certain espace, o une
ventuelle symphyse puisse se produire sans
intresser la partie malade, qui doit tre
maintenue en collapsus. Malgr les
dcollements massifs, on pourrait dire mme
totaux, nous navons jamais eu un cas de
dyspne avec cyanose cause de la
rduction du champ dhmatose.
Cest bien entendu, quon a toujours
dtermin la capacit respiratoire des
malades et que le poumon oppos doit tre
sans lsions. La diminution de la capacit
respiratoire aprs la pneumolyse peut tre
contrle par le spiromtre de Gaubatz.
Les avantages de ces modifications
techniques:
1. Une petite cicatrice avec situation
basse, cache et qui ne porte pas le
stigmate de la maladie.
2. Un grand dcollement qui permet aussi
de collaber les lobes infrieurs,
agrandissant ainsi le chapitre des

indications qui peuvent bnficier de


cette mthode.
3. Le procs de symphyse est beaucoup
retard et donc on peut entretenir la
poche cre, seulement avec de lair,
sans avoir besoin dinstituer un olothorax antisymphysaire.
Complications:
Lhmorragie
Lhmorragie dans la cavit provient,
dans la majorit des cas, des veines
perforantes intercostales et des branches de
la mammaire interne (Maurer).
En gnral nous avons eu une
hmorragie parenchymateuse ngligeable.
Au cas o il survient aussi une hmorragie
dune artre ou dune veine, il faut larrter
par
une
ligature
ou
une
diathermocoagulation. On emploie, dans ce
but les cautres de la trousse Jacobaeus.
Les symptmes de lhmorragie
apparaissent dans les premires 6-12 h,
parfois mme 24 h, et se manifestent par
lacclration du pouls, la diminution de la
quantit dhmoglobine, pleur et dyspne,
due llvation de la pression intracavitaire
et au dplacement du mdiastin et parfois
mme un emphysme sous-cutann.
En gnral lhmorragie nest pas
abondante et peut tre arrte par les
hmostatiques habituels: Clauden, Glatine,
Calcium, et des transfusions. Lhmorragie
sarrte dhabitude par auto-tamponnade,
sagissant dune cavit close. Nanmoins
aprs les larges dcollements que nous
pratiquons, nous avons eu un cas o, aprs 8
heures, il a fallu intervenir de nouveau en
vacuant lhmatome et en tamponnant la
cavit avec des compresses strilises
pendant 48 h.
Cest
pour
cela
que
nous
recommandons,
comme Schmidt, la
dtermination des groupes sanguins des
malades, avant lopration, pour pouvoir
intervenir temps en cas dhmorragie, par
des transfusions jusqu 500 cm- et parfois
mme rptes.

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Jurnalul de Chirurgie (Iai), 2013, Vol. 9, Nr. 2

Les ponctions se font dhabitude le 9me-10-me jour aprs lintervention,


lorsque lhmatome est ramolli.
En certains cas, lorsquil sagit dun
dplacement mdiastinal ou une trop grande
pression (+20 et mme plus), on peut les
faire plus tt.
La dissolution du coagulum est faite
par des lavages dacide borique ou du srum
physiologique.
Lhmatome donne, dans certains cas,
de la fivre jusqu 38, mais sans indiquer
une infection, sagissant dune temprature
de rsorption.
Les ponctions se font toujours dans la
partie suprieure, pour ne pas lser le
poumon collab. Elles sont rpter chaque
fois que lexamen radioscopique nous
indique lexsudat ou dans le cas o la
temprature monte.
Le contrle radioscopique doit tre fait
chaque semaine et, parfois, mme plus
souvent.
Schmidt a fait construire une chaise
rotative qui permet de donner au malade
toutes les inclinaisons, de sorte quil puisse
vacuer lexsudat.
Les ponctions doivent tre faites avec
un trocart ou une aiguille ponctions, plus
grosse. La quantit dexsudat que nous
avons extraite le 9-11-me jour, a vari entre
300-900 cm. Lexsudat doit tre toujours
examin du point de vue bactriologique et
cytologique.
Lhmorragie apparait parfois, mme
aprs plusieurs semaines, dans la poche
cre, mais sans tre massive, et daprs
Schmidt, est probablement en rapport avec le
facteur local, la saison et les variations
atmosphriques.

On recommande dans ces cas, comme


traitement, le lavage la solution dacide
borique. Ces suppurations abactrienne sont
trs vite guries.
Les
suppurations
bacillaires
surviennent, daprs Schmidt, en 4% des cas.
Nous en avons eu jusqu prsent 4%. Elles
sont dues louverture des vaisseaux
lymphatiques, louverture des procs
bacillaires par des vaisseaux pleuraux
microscopiques et louverture des cavernes
dans
la
cavit
extra-pleurale.
On
recommande comme traitement des lavages
au
Presoyode,
Dijozol,
Cloramine,
Trypaflavine, Rivanol, Gomenol etc. Ces
suppurations sont dhabitude de longue
dure et elles mnent une symphyse qui
ncessite ultrieurement une thoracoplastie.
Dans les cas dinfection mixtes, on
recommande douvrir largement la cavit
cre.
Les
suppurations
cocciques
surviennent gnralement en 15% des cas,
dont 13% sont des suppurations septicotoxiques et 25% sont des suppurations
bnignes (Schmidt). Les suppurations
cocciques surviennent dhabitude la suite
des ponctions post-opratoires, faites soit
pour vacuer lexsudat, soit pour les
insuflations, mais o lon a nglig les
prcautions aseptiques ou mme la suite
des perforations des cavernes dans la cavit
extra-pleurale.
Elles sont dues au staphylocoque et au
streptocoque hmolytique. Leur traitement
est long et exige beaucoup de patience autant
de la part du malade, que du mdecin.
Daprs Schmidt, 44% des cas sont guris
permettant de continuer les insufflations,
tandis que le reste aboutit la thoracoplastie.

Les suppurations
Schmidt divise les suppurations qui
peuvent se produire dans la cavit cre en
trois groupes: suppurations sans bactries; 2)
suppurations bacillaires; 3) suppurations
cocciques. Les premires sont dues la
raction de la paroi ainsi que par la
rsorption du coagulum et louverture des
voies lymphatiques.

Les fistules
Elles sont dues aux infections
pntrantes de la plaie opratoire et se
ferment la fin de la suppuration.
Une complication assez rare, que
Schmidt ne rappelle pas dans son trait et
que nous avons eu, cest la bronchopneumonie caseuse dans le poumon collab
et qui est gnralement fatale.

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Jurnalul de Chirurgie (Iai), 2013, Vol. 9, Nr. 2

La mortalit
Nous avons
mortalit de 4%.

jusqu

prsent

une

Conclusions
Le
pneumothorax
extra-pleural
constitue une nouvelle conqute de la
chirurgie, dans le domaine de la
collapsothrapie. Cest une mthode
relativement rcente et propos de laquelle
la physiologie na pas encore prononc son
dernier avis.

Il faut pourtant avouer quelle se fraye


son chemin et que, malgr ses complications
parfois redoutables, elle donne de trs bon
pourcentage de bacilloscopie ngative, pour
ne pas dire des gurisons, mot trop os pour
la tuberculose pulmonaire.
Malgr tout cela, les progrs raliss
par la chirurgie thoracique nous autorisent
esprer que, dans un avenir pas trop loign,
nous aurons la surprise de voir devenues
extirpables les lsions bacillaires tendues,
mais limites seulement un ou deux
lobes.

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COMENTARIU LA ARTICOLUL:
CONTRIBUTIONS LA TECHNIQUE DU
PNEUMOTHORAX EXTRA-PLEURAL - 75 CAS OPRS
C. Crpiniam, M. Onceso - Revista de Chirurgie 1940; 9-10/43: 671-679.
Nicolae M. Constantinescu
Universitatea de Medicin i Farmacie Carol Davila Bucureti

n afara unei nevoi fireti de


diversificare a tematicii abordate prin
scoaterea la lumin a unor lucrri fcute la
nivelul toracelui de ctre chirurgii romni n
urm cu 73 de ani, am socotit necesar s
readuc n memoria chirurgilor generaliti
figura lui Cornel Crpinian (1904-1970)
considerat pe drept cuvnt fondatorul
chirurgiei toracice clinice i experimentale
din ara noastr.
Chirurg desvrit, exigent cu el nsui
i cu colaboratorii Cornel Crpinian a fost
profesor la Facultatea de medicin din
Bucureti ntre 1949-1969, n care timp a
format o adevrat coal de chirurgi
toracici.
Faptul c ntre 1938 i 1940 a lucrat la
Sanatoriul de tuberculoz de la Moroieni l-a
apropiat de aceast patologie, care la vremea
aceea era nc un flagel greu de stpnit.
Menionm spre exemplu c n Frana, n
1918, 1/6 din bolnavi decedau n urma
tuberculozei (Wikipedia).
Negativarea sputei i apoi sterilizarea
focarului tuberculos pulmonar au putut fi
obinute la bolnavii cu caverne bacilare dup
introducerea de ctre Forlanini n 1882 a
pneumotoraxului terapeutic; el constatase

Adresa de coresponden: Prof. Dr. N.M. Constantinescu


Universitatea de Medicin i Farmacie Carol Davila Bucureti
E-mail: nae_constantinescu@yahoo.com

colabarea unei caverne pulmonare ca urmare


a unui pneumotorax spontan.
Imobilizarea
pulmonului
infectat
comprimat prin aerul introdus, permitea n
continuare organismului s vindece leziunea
tuberculoas.
Cornel Crpinian introduce n
Romnia la Moroieni pneumotoraxul
extrapleural executat sub anestezie locoregional nregistrnd o mortalitate de 4%.
Imaginile radiografice ne arat
dispariia cavernelor, ceea ce contribuia la
ntreruperea ciclului evolutiv al infeciei
bacilare.
Cornel Crpinian ni se demonstreaz
ca un desvrit tehnician, imaginativ i
raional.
Opiunea
pentru
abordul
extrapleural i-a conferit o mare libertate de
manevr n interiorul cutiei toracice, iar
tehnica a dezvoltat-o n 1941 n monografia
dedicat
toracoplastiei
cu
apicoliz
extrafascial.
Odat
cu
introducerea
tuberculostaticelor
morbiditatea
i
mortalitatea prin tuberculoz au sczut
dramatic, motiv pentru care i colapsoterapia
a fost reconsiderat.

NOUTI

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Jurnalul de Chirurgie (Iai), 2013, Vol. 9, Nr. 2

EUROAMERICAN MULTISPECIALITY SUMMIT VI


Laparoscopy & Minimally Invasive Surgery
Disneys Contemporary Resort, Orlando, Florida, U.S.A., February 13-16, 2013

VI

February 13-16, 2013

n perioada 13-16 februarie 2013 s-a


desfurat n Orlando, Florida, S.U.A.,
Summitul Euro-American dedicat chirurgiei
minim invazive. Ajuns la a 6-a ediie,
manifestarea organizat din doi n doi ani, de
prestigioasa Societate a chirurgilor laparoendoscopiti (Society of Laparoendoscopic
Surgeons SLS) se bucur de un real
succes; de altfel, SLS organizeaz alternativ,
tot in februarie, o replica asiatic, AsianAmerican Summit, n Hawaii.
Obiectivul reuniunii este de a asigura
un schimb de experien chirurgical dar i
cultural
ntre
membrii
comunitii
chirurgicale de pe un mal i de pe altul al
Atlanticului.

Ceremonia de deschidere /
P.A. Wetter, preedintele SLS
www.sls.org

Manifestarea a debutat printr-o


Ceremonie de deschidere n care Romnia a
ocupat un loc special, fiindu-i rezervat o
prezentare cultural (cultural presentation)
(Dr. C. Tiu). Expunerea s-a axat pe tradiia i
deschiderea cultural a Romniei i s-a
ncheiat cu invitaia adresat plenului i
boardului SLS de a vizita Bucuretiul n
iunie
2015,
atunci
cnd
Palatul
Parlamentului va fi gazda Congresului
International EAES.
O a doua prezentare cultural a fost
susinut de Dr. M.E. Orady (S.U.A.)
Islam and Muslims in the West - tema fiind
de mare actualitate n contextul geopolitic
actual.
Programul tiinific a debutat pe 14
februarie printr-o serie de conferine axate
pe importana trainingului n chirurgia
minim-invaziv: First preclinical and
clinical results of a novel European
telesurgical system with haptic sensation
(M. Stark, Germania), Laparoscopic
surgical trening a three stages model (R.
Moldovanu, Romnia), Advantages of new
instrumentation
for
more
precise
laparoscopic surgery in 2013 (L. Mettler,
Germania), New technology for surgery
energy directed surgery: Will it replace
current surgical practice? (R. Satava,
S.U.A). Una dintre cele mai interesante
prelegeri a aparinut preedintelui SLS, Prof.
P.A. Wetter (S.U.A.) Improve the
outcomes for six milion surgical patients
OR Ready iniiativ a SLS ce are n vedere
implementarea conceptelor de warm-up i
generalizarea check-list n spitale, pentru a
mbunti
performanele
echipelor
chirurgicale i securitatea pacientului. De
altfel, principiul OR Ready este sintetizat
astfel: SLOW DOWN for WARM UP and

204
Jurnalul de Chirurgie (Iai), 2013, Vol. 9, Nr. 2

CHECK LISTS ! STOP for TIME OUT


before you GO !.
Detalii despre programul OR Ready
sunt
disponibile
pe
site-ul
SLS:
http://laparoscopy.blogs.com/outcome/.
Programul de dup amiaz a fost a fost
dedicat unei sesiuni black video, Surgical
surprises, accidents and complications - To
err is human, to carrest is master surgeon
avnd drept motto Now how do I get out of
this? Sesiunea a fost moderat de CH. Koh
avnd drept comentatori celebri chirurgi din
America: MK Chung, M. Gagner, WE
Kelley Jr, L. Metter, JB Petelin, JA Redan,
JC Butch Rosser, RM Sweet.
Programul zilei de vineri, 14 februarie,
s-a adresat chirurgilor de diferite specialiti,
sesiunile de chirurgie general alternnd cu
cele de urologie i ginecologie. Trebuie
menionate conferinele: Learning curve in
single-incision laparoscopic cholecystectomy
(A.M. Onate, Mexic), Minilaparoscopy or
single port? (G.L. Carvalho, Brazilia),
Laparoscopic
choledoscopy
in
the
management of bile duct stones (A.S.
Kawashti, Egipt), Laparoscopic treatment of
diverticulitis Hinchey 3 (F. Lattanzio, Italia),
Laparoscopic sleeve gastrectomy: long term
results (M. Gagner, Canada), Learning curve
for resident training in laparoscopic

intestinal anastomoses (J.I.M. Parra,


Spania). Programul de dup amiaz a fost
rezervat unei sesiuni n limba spaniol
pentru chirurgii din America de Sud i
Central.
Din programul zilei de smbt, 16
februarie, trebuie menionate lucrrile: The
ESSCL electronic checklist (N. Pairaudeau,
Canada), Complications of TAPP procedures
for groin hernia (L. Sakra, Cehia), Novel
treatments for post hernia repair and
testicular pain: nuts, bolts and robots (S.
Parekattil, S.U.A.), Financial aspects of
laparoscopic hepatectomy (A. Kyritsis,
Grecia), Focused ultrasound therapy the
transfer of techniques towards moving
organs (C. Tiu, Romnia), Overview of
robotic hysterectomy in benign gynecology
(M. Orady, S.U.A.).
Reuniunea s-a ncheiat cu nmnarea
diplomelor de participare i a certificatelor
de acreditare CME.
Programul manifestrii i rezumatele
lucrrilor sunt disponibile online la adresa:
http://laparoscopy.blogs.com/ea07/upcoming
-summit-euroamerican-2013/ .

Dr. R. Moldovanu
Dr. C. Tiu

Copyright JURNALUL DE CHIRURGIE (Iai) 2005-2013