Azienda Ospedaliera Papa Giovanni 23° - Bergamo · PDF fileAzienda Ospedaliera Papa...

Azienda OspedalieraPapa Giovanni 23° - Bergamo

Fondazione per la Ricerca Ospedale Maggiore di Bergamo - FROM

Le infezioni delle vie biliariA cura dell’USC di Malattie Infettive,

con la collaborazione di:

-USC Chirurgia 1-USC Chirurgia 3-USC Endoscopia digestiva – Gastroenterologia 2-USC Gastroenterologia 1-USC Microbiologia-USS Radiologia Interventistica Presentato Novembre 2014

Caso clinico 1: febbre e addominalgie

Paziente BP, donna, 91 anni

Diabete mellito, ipertensione arteriosa, FA (warfarin)

Addominalgie, nausea e vomito, febbricola

GB 16380/mmc (N 88,4%), creatinina 1,34 mg/dL, AST/ALT 19/14 U/L, PCR 5,9 mg/dL

Rx addome: non livelli idro-aerei, non aria libera.

RICOVERO IN MALATTIE INFETTIVE

All’ecografia addome: marcataidrope della colecisticon pareti nettamente ispessite(fino a 1 cm) contenenteun calcolo infudibolare di 2-3 cm… non dilatazione VB …

VALUTAZIONE CHIRURGICA

Caso clinico 1:febbre e addominalgie

“In conclusion I wish to express the hope that some daysurgeons will be fairly unanimous in their views on thetreatment of acute inflammations of the gall-bladder.”

Ann Sur. 1928

La storia

Situazione

•Meta-analisi (Papi 2004 e Gurusamy 2013)•Linee guida internazionali TG07 – TG13

� COLECISTECTOMIA IN URGENZA!!!

• 60-80% dei chirurghi preferisce approccio conservativo (Senapati 2003,Askew 2005, Campbell 2008)

• Solo il 40% di pazienti riceve trattamento al primoepisodio (Badia 2014)

�Analisi retrospettiva – dati amministrativi

� Ricoveri urgenti

� Codici SDO colecistiti + codici DRG(escluse colangiti e pancreatiti)

� Data base ASL Bergamo - Successivi ricoveri e follow-up

� 1 gennaio 2008-30 aprile 2013

� Cambio organizzazione: maggio 2010

Materiali e metodi

502 pazienti 62.09 anni 56.2% maschi

Charlson’s comorbidity index 3

Risultati

Risultati per trattamento

p<0.0001p<0.0001


•1,03 vs 2,13 accessi in ospedale

•Guadagno di 5,3 giorni di degenza

•2263 € risparmio per la struttura

•Non complicanze aggiuntive


+751 €

-431 €

Analisi del timing operatorio early

p<0.0001p<0.0001

p=NSp=NS

Risultati per periodo

2 periodi individuati 01/1/08-31/5/10 e 1/6/10 -30/4/13Gruppi omogenei per caratteristiche demografiche

Risultati per periodo

p<0.0001p<0.043

Risultati per periodo early

p=NS

p=NS

Papa Giovanni XXIII Hospital Scenario•2 Surgeons on call•H24 Operating Room (not exclusively dedicated to our unit)•Level I Trauma Center•Sugical Unit activity: mix case of upper and lower GI surgical oncology,advanced surgical oncology acute care surgery

ACC: Colecistite Acuta Calcolosa

The HPG23 Protocol for the Treatment of ACC

Tokyo Guidelines

2013

ASGE e SAGES

Guideline J

GASTROINTESTINAL

ENDOSCOPY Volume

71, No. 1 : 2010 1-9

P-Possum Score e

Giudizio Clinico

http://berian.altervista

.org/portale/ppossum

ACC DIAGNOSISA) Local Sign of inflammation

• Murphy’s Sign• RUQ pain/mass/tenderness

B) Systemic Sign og inflammation

• Fever (not defined)• Elevated CRP (not defined)

• Elevated WBC count (not defined)

C) Imaging findings Imaging characteristic of Acute Cholecystitis

Definite Diagnosis

one item in A + one item in B+ C

1

ACC?

AbdominalUltrasound

•Biliary stones/sludge•Wall thickness: =5mm•Fluid collection around

cholecystitis•Ultrasound Murphy

If possible obtain stonessize(=5mm)

CONFERMA di SOSPETTO di CALCOLOSI DELLA VIABILIARE PRINCIPALE

Fattori Predittivi di Coledocolitiasi

CVBP evidenziati all’ecografia transaddominale

MOLTO FORTI Colangite ascendente Bilirubina > 4

FORTI

Coledoco > 6 mm (con colecisti in sede)

Bilirubina tra 1.8 e 4

MODERATI

Anormalità dei test epatici differenti dalla Bilirubina

Età>55 aaPancreatite biliare

Classi di Rischio per Coledocolitiasi

ALTA

Presenza di uno dei “FATTORI PREDDITIVI MOLTO FORTI”

Oppure

Presenza di entrambi “FATTORI PREDITTIVI FORTI”

BASSA

Assenza di FATTORI PREDITTIVI

INTERMEDIA

TUTTI GLI ALTRI CASI

2

Sospetti

Calcoli via

biliare

?

ERCP

NIENTE

Ecoendo

vs.

Colangio RM

QUALE TRATTAMENTO PER LA LITIASI VIA BILIAREIN COLECISTITE CALCOLOSA?

http://www.triveneta.org/slides/Trieste240911/02-roseano.pdf

3

Candidato a

Intervento?

CUT-OFF DI MORTALITA’ 10%

� Risorse Umane/Strumenti:

� Chirurgo-Anestesista Sala Operatoria H24 (Strumenti: P-Possum Score

http://berian.altervista.org/portale/ppossum/ , Giudizio Clinico)

� Disponibilità attuale: Sì.

� Risorse aggiuntive: NO

Pronto Soccorso/Medicina Urgenza/Gastro2

3

Candidato a

Intervento?

3

Candidato a

Intervento?

NO

Risorse Umane/Strumenti:

Chirurgo-Anestesista Sala Operatoria

H24 (Strumenti: P-Possum Score

http://berian.altervista.org/portale/ppos

sum/ , Giudizio Clinico)Disponibilità attuale: SìRisorse aggiuntive: NO

Pronto Soccorso/Medicina Urgenza/

Gastro2

3

Candidato a

Intervento?

NO

ANTIBIOTICOPER 48 ORE

FALLIMENTOATB?

SI

COLECISTOSTOMIA


Medico-Infermiere Med Urg; Medico-

Infermiere Gastro 2; Radiologo Interventista

(Strumenti: Antibiotici, Ecografia

interventistica)Disponibilità attuale: SìRisorse aggiuntive: NO

Medicina Urgenza/Gastroenterologia 2

3

Candidato a

Intervento?

NO

ANTIBIOTICOPER 48 ORE

FALLIMENTOATB?

SI

COLECISTOSTOMIA

FALLIMENTOCOLECISTOSTOMIA?

INTERVENTO


Medico-Infermiere Med Urg; Medico-Infermiere

Gastro 2; Radiologo Interventista, Chirurgo-

Infermiere Chir 1; Anestesista-Personale Sala H24

(Strumenti: Antibiotici, Ecografia interventistica, Sala

Operatoria H24)Disponibilità attuale: SìRisorse aggiuntive: NO

Medicina Urgenza/Gastroenterologia 2/

Chir 1

ColecistiteVia Biliare

Selezione Paziente

Colecistite + VBP-:•Candidato ad intervento: Intervento urgenza differibile (Gestione Chirurgia 1)•Non candidato ad intervento: Antibiotico, eventuale colecistostomia (Gestione Medicinad’Urgenza; eventuale intervento se colecistostomia inefficace)

Colecistite + VBP+:Studio e terapia VBP: Ecoendo, Colangio RM eventuale ERCP (Gestione Gastroenterologia 2)•Candidato ad intervento: Intervento urgenza differibile (Gestione Chirurgia 1)•Non candidato ad intervento: Antibiotico, eventuale colecistostomia (GestioneGastroenterologia 2; eventuale intervento se colecistostomia inefficace)


La paziente non ha indicazioni chirurgicheha già eseguito emocolture

Quale terapia antibiotica empirica?

Tempestiva CorrettaOttimizzata

Tokyo Guidelines 2013for acute cholangitis and acute cholecistitis

La terapia antibiotica va iniziata non appena si sospetti un’infezione biliare

Entro un’ora se shock settico

Entro 4 ore nei pazienti stabili

Previa esecuzione di emocolture

J. Hepatobiliary Pancreat Sci (2013) 20: 60-70

Terapia antibiotica empirica corretta

Quale molecola?

- Spettro d’azione compatibile con il sospetto clinico- Adeguata penetrazione nel sito di infezione- Pattern di resistenza locale- Fattori dell’ospite

Considerare i focolai eradicabili

Quale dose ?

- dose carico antibiotici- dose di mantenimento

Isolamenti microbiologici da bilee sangue nelle infezioni acute biliari

J. Hepatobiliary Pancreat Sci (2013) 20: 60-70

Isolati bile % sangue %

Gram negativi

Escherichia coli 31-44 35-62Klebsiella spp 9-20 12-28Pseudomonas spp 0,5-19 4-14Enterobacter spp 5-9 2-7

Gram positivi

Enterococcus spp 3-34 10-23Streptococcus spp 9-20 6-9Anaerobi 4-20 1

Penicilline Ampicillina, piperacillina, pipera/tazo

Cefalosporine1° gener. Cefazolina2° gener. Cefmetazolo, cefotiam3° gener. Cefoperazone/sulbactam, ceftriaxone,

ceftazidime

Fluorchinoloni Ciprofloxacina

Monobattami Aztreonam

Carbapenemi Meropenem

Lincosamidi Clindamicina

Antibiotici ad elevata concentrazione biliare/colecistica

Hepatogastroenterology 1996; 43: 800-6

Gicilcicline Tigeciclina

E’ necessario utilizzarli?

Van den Hazel, CID1994 Aug;19(2):279-86, WSES Guidelines 2013, TG 2013

L’escrezione antibiotica biliare si fermase vi è ostruzione biliare

La terapia può fallire se non è associata alla disostruzione delle VB

Non è strettamente indispensabile

Terapia antibiotica empirica dellecolecistiti/colangiti: il protocollo aziendale

COMUNITARIA OSPEDALIERA

Sepsi graveSepsi grave

No sepsigrave

Pip +Tige+/-

Fluco

Mero-(Imi-Dori)

+/-Vanco

+Echino

ESBL +ESBL -

No sepsigrave

Amoxi/clav

Cipro +

metro

Pip/tazo

Se allergiaTigeciclin

a

Adattato da WSES Guidelines 2013, TG 2013

OO.RR.BG/HPG23:bacilli G-isolati da bile – 2012/14

10

9

15

E. coli K. Pneumoniae Altri

34 isolati positivi di cui 5 ESBL produttori

(14,7%)

3/34 produttori di carbapenemasi

(8,8%)

Microbiologia HPG23: dati dal 1/1/2012 al 31/03/2014

Come identificare i pz a rischio x ESBL?

Tumbarello M. et al.: Antimicrob. Agents Chemother. July 2011, 3485-3490

Attribute No. of points

Recent antibiotic therapy with beta-lactams a

and/or fluorquinolones 2

Previous ospitalization b 3

Transfer from another healthcare facility 3

Charlson comobidirty score > 4 2

Recent history of urinary catheterization c 2

Age > 70 years 2

a During the 3 months preceding the index hospitalizationb During the 12 months preceding the index hospitalizationc During the 30 days preceding the index hospitalization

Score ≥≥≥≥ 3: ESBL carrier possible

Start with tigecicline or carbapenem then shift if notconfermed

Score ≥≥≥≥ 8: ESBL high probable

Start with tigecicline or carbapenem.The patient should be isolated.

Come identificare i pz a rischio xESBL?

Tumbarello M. et al.: Antimicrob. Agents Chemother. July 2011, 3485-3490Jhonson SW. Et al: Infect Control Hosp Epidemiol 2013 April; 34(4): 385-392

Durata della terapia antibiotica:da WSES 2013 e TG 2013

Se la fonte di infezione è controllata:4-7 gg

Se colecistectomia: stop terapia dopo 24 ore dall’intervento

Se sepsi da Enterococcus spp o Streptococcus spp:14 gg

WSES Guidelines 2013, TG 2013,


La paziente è stata trattata conpiperacillina/tazobactam4,5 g in SF 100 cc x 3/die

Dimessa in riabilitazione(16 gg di degenza)

Miglioramento clinico

Miglioramento ecografico

Terapia antibiotica

- tempestiva- corretta- ottimizzata

+

Disostruzione

(se stasi l’antibioticonon viene escreto

nelle VB)

Westphal J-F and Brogard JM, Drugs 1999 Jan; 57 (1): 81-91

Conclusione 1:infezione acuta delle vie biliari

Scopo del trattamento è bonificare il sito di infezione

Caso clinico 2:colangiti febbrili recidivanti

Paziente VL, uomo, 63 anni

16/02/2009: OLTx per cirrosi HBV-HDV correlataAnastomosi bilio-biliare T-TImmunosoppressione: FK + steroide

Maggio 2009: indici di colestasi elevati All’ERCP: stenosi serrata dell’anastomosi a livello del dotto epaticocomune, sfinterotomia, dilatazione pneumatica e posizionamentodi endoprotesi biliare


Giugno 2009: nuovo ricovero percolangite.

Rimossa per via endoscopica la protesibiliare (non ostruzione)


26/08/2009: nuovo ricovero per febbre,all’ERCP stenosi serrata dell’anastomosi

+ coledocolitiasi della VB pre-anastomotica


30/11/2009: all’ERCP rimossaendoprotesi biliare precedente,

posizionatadoppia endoprotesi


Gennaio 2010Confezionamento di anastomosi

bilio-digestiva su ansa Ypresso la Chirurgia 3

Persistenza di episodi febbrilida enterobatteri

Acute Cholangitis: Definition

Acute Cholangitis: A morbid condition with acuteinflammation and infection in the bile ducts. It results froma combination of biliary obstruction and bacterial growth inthe bile.

Charcot’s triad (1877):�Chills�Right upper quadrant abdominal pain�Jaundice�Reynold’s Pentad (1959):�Lethargy or mental confusion�Shock�Fever�Jaundice�Abdominal pain

Jean Martin Charcot

Acute Cholangitis: Pathophysiology

Under physiologic conditions, several mechanisms are involved inmaintaining the sterility of bile.

�Bile salts have bacteriostatic properties.

�The sphincter of Oddi controls the direction of bile flow and serves as abarrier between the sterile bile duct and the nonsterile duodenum.

�Infection results from bacterial colonization of the biliary system.

�Gram – bacteria (Escherichia Coli, Klebsiella spp) and Gram +enterococci are commonly found in biliary cultures.

�Enterobacter, Proteus, Pseudomonas, and Bacteroides spp, are lessfrequently isolated from bile.

Mosler P Curr Gastroenterol Rep 2011, 13:166-172


The onset of acute cholangitis involves:

�Increased bacteria in the bile duct

�Elevated intraductal pressure in the bile duct allowingtranslocation of bacteria or endotoxin into the vascular andlymphatic system (cholangio-venous/lymphatic reflux)

�Translocation of bacteria into the bloodstream results insepticemia, an often fatal complication of acute cholangitis


� Colonization of a biliary system by bacteria in the absence of obstruction(i.e. infected but not obstructed) does not usually progress to clinicalcholangitis.

� It is not always obvious how bacteria enter an obstructed biliary system,unless interventions such as surgery, ERCP, PTC have been performed,resulting in loss of the physiologic barrier between the bile duct andintestine.

� Patients with incomplete biliary obstruction have been shown to have ahigher positive bile culture rate than those with complete obstruction.

Mosler P Curr Gastroenterol Rep 2011, 13:166-172

Acute Cholangitis: Etiology

Acute cholangitis: Clinical Presentation

The typical clinical picture of Charcot’s triad is not alwayspresent in patients with acute cholangitis, and further diagnostictesting may be required before the diagnosis can be established.

�Fever and abdominal pain 80%

�Jaundice 60-70%

�Shock and altered mental status 3,5-7%

Acute Cholangitis: Diagnostic Criteria

� Standard diagnostic criteria for acute cholangitis have beenlacking, and various definitions for the disease have been usedin the past.

� The “Tokyo Guidelines” recently recommended a moresystematic approach, using a combination of clinical features,laboratory data, and imaging findings to diagnose acutecholangitis.

� Tokyo Guidelines 2007 ? 2013

Acute Cholangitis: Diagnostic Criteria

Tokyo Guidelines 2013 J Hepatobiliary Pancreat Sci 2013;20:24-34

Acute cholangitis: Diagnostic Imaging

Acute Cholangitis:Therapeutic Management

The therapy of acute cholangitis is directedtoward the two main etiologic components ofthe disease:

�Biliary infection ? Systemic antibiotics

�Biliary obstruction ? Biliary drainage

�Appropriate supportive care

Biliary Drainage

�ERCP +ES + PS or SEMS placement

�PTBD

�Trans-duodenal papillo-sphincterotomy/sphincteroplasty

�Roux en Y Hepaticojejunostomy

Acute Cholangitis:Therapeutic Management

Loop length 50-70 cm

Acute cholangitis: Clinical Presentation

Tokyo Guidelines 2013, J Hepatobiliary Pancreat Sci 2013, 20:24-34

Flowchart for the management of acute cholangitis

Miura F, J Hepatobiliary Pancreat Sci 2013, 20:47-54

Biliary Strictures after OLTx

• Anastomotic Strictures

• Non Anastomotic Strictures

Vascular supply of the biliary tract and clinicalimplications for OLTx

� Bile ducts are supplied only arterially.

� Biliary epithelium is more liable to ischemic injurythan hepatocytes.

� Severe hypotension eventually leads to an “ischemiccholangiopathy” with biliary necrosis, cast formation,subsequent scarring and multifocal stenosis.

Biliary complications after OLTx

D Seehofer et al. Am J Transpl 2013;13:253-265

Anastomotic Strictures (AS)

Definition: A dominant narrowing at the anastomotic site, withouteffective passage of contrast material, as identified bycholangiography. They result mainly from surgical technique andlocal ischemia, leading to fibrotic scarring of the anastomosis.They involve choledocho-choledochostomy or choledo-chojejunostomy. They are single and short in length.

Incidence: 13% (full size graft)

19% (split and LDLT)

Early Strictures: Those diagnosed

within 1 month after transplantation.

Late Strictures: Those diagnosed

1 month or longer after transplantation.

Anastomotic Strictures (AS): Risk Factors

� Excessive dissection of peri-ductal tissue during procurement.

� Excessive use of electro-cautery for biliary duct bleeding controlin both donor and recipient.

� Tension of the duct anastomosis.

� Small bile leaks resulting in a peri-anastomotic fibro-inflammatory response.

� Ischemia at the end of the bile duct resulting in fibro-proliferative response.

� Early HCV recurrence (16%AS vs 6% late HCV recurrence)

Krok KL et al Clin Liver Dis 2010;14:359-371

Anastomotic Strictures (AS): Diagnostic Approach

� US with doppler evaluation of hepatic vessels

� Angio CT or hepatic angiography

� ERCP

� PTC

� MRCP

� Liver Biopsy

� ERCP balloon dilatation and plastic stent placement

� ERCP balloon dilatation and full covered expandablemetal stent placement

� PTC + external/internal biliary drainage ±expandable metal stent placement

� Roux en Y hepatico-jejunostomy

Anastomotic Strictures (AS): Therapy

OLTx within 3 months or more than 5mg ofprednisone per day:

�Dilation with a 10F biliary dilator, and a 10 Fstent placed for 12 weeks

�During a subsequent ERCP. The stent wasremoved and balloon dilation was performedwith a balloon (6-10 mm diameter) for 1minute.

�A sphincterotomy was performed with thestandard technique and a maximal number (upto 9) of 8,5F to 11,5F stents were placed acrossthe anastomosis

OLTx more than 3 months and less than 5mgof prednisone per day:

�Initial ERCP with 1 minute balloon dilationfollowed by placement of the maximal numberof stents at the initial and subsequent ERCP

Follow up:

�Liver function tests and clinical evaluationevery 12 weeks

�Only 1 or 2 stents in place ? ERCP at 3months intervals or earlier if signs or symptomsof biliary obstruction

�3 or more stents in place ? ERCP and stentexchange only when signs or symptoms ofbiliary obstruction or after 1 year without stentexchange, whichever came first

Group A: PCMS Partially Covered Metal Stent diameter 10 mm Length 60,80,100 mmGroup B: FCfins Fully covered with fins; diameter 10 mm, length 40,60,80,100 mmGroup C: Fcfe Fully covered with flared ends; diameter 10 mm, length 60,80 mm

Gastrointestinal Endoscopy, 2013;77(5):679-691


Conclusion I�There are no RCTs or NRCTs that directly compare BD +MPSs vs CSEMSs

�CSEMSs offer the advantages of longer stent patency (compared with asingle PS) and easy removal.

�Both strategies have very high technical success rates and low adverse eventrates in ABSs of OLT patients, despite the need for multiple ERCPs perpatient.

�A much lower stent migration rate with MPS compared with a single PS andcovered SEMS have been reported

�MPSs with a minimal stent duration of 12 months and CSEMS with a minimalstent duration of 3 months had similar ABS resolution rates after OLTx

�Current evidence does not suggest a clear advantage of SEMS use over MPSsin the management of ABSs after OLTx


Conclusion II•What are the optimal stent protocol and stent duration ?

•Should covered SEMSs be used early or only in cases in which a trial of MPSshas failed ?

•Is an SEMS duration as long as 6 months safe and feasible, and can it replacemultiple sessions of BD and PS placement ?

•Does early use of SEMSs reduce the number of ERCPs required per patient,improve outcomes, and is cost-effective compared with MPSs ?

•Results of randomized trials comparing PSs and SEMSs may offer furtherclarification

Non Anastomotic Biliary Strictures (NAS)

Definition: NAS are strictures at any location in the biliarysystem of the transplanted liver (intrahepatic or extrahepatic).First described after OLTx as a cholangiographic image of biliarystrictures and dilatations caused by ischemia after HAT.However, such cholangiographic abnormalities of strictures anddilatations can also be seen in patients who do not have HATand the name first given to this last subgroup of strictures was“Ischemic Type Biliary Lesions” ITBL.

Incidence: 1-20%

Time interval from OLTx: 0,3 – 155 months

Early NAS: < 1 year from OLTx

Late NAS: > 1 year from OLTx

Transplantation 2011;92:373-379


� Bile ducts entirely depend on arterial blood supply foroxygenation

� Cholangiocytes are highly susceptible to reoxygenation afteranoxia (reperfusion injury)

� In DCD warm ischemia time in the donor in addition tosubsequent cold-ischemia reperfusion injury is believed toresult in increased damage to biliary epithelial cells

� Insufficient flush out of the microvasculature of the liver(peribiliary capillary plexus) is believed to play a role in thedevelopment of NAS

Transplantation 2011;92:373-379


Zone A: Hilar bifurcationZone B: Ducts between the first- and second- order branchesZone C: Ducts between the second-and third- order branches

Zone D: Periphery of the liver


Early (< 1 year)

Location: bile ductbifurcation and extrahepaticbile duct.

Mechanism: Ischemiamediated (longer cold andwarm ischemia)

Late (> 1 year)

Location: more frequently inthe periphery of the liver.

Mechanism: Immune-mediated



Mild NAS Moderate NAS

Severe NAS Buis CI et al Liver Transplant 2007;13:708-718

Non Anastomotic Biliary Strictures (NAS):Risk Factors

Early NAS (= 1 year)�Prolonged CIT (> 12 hrs)

�Prolonged WIT (> 60 min)

�Viscosity and perfusionpressure of preservationsolution

�Cytotoxic effect ofhydrophobic bile salts

�DCD

Late NAS (= 1 year)�F-M D-R match

�PSC as indication for OLTx

�AB0 incompatibility

�CMV infection

Buis CI et al Liver Transplant 2007;13:708-718

Non Anastomotic Biliary Strictures (NAS):Treatment Options

D Seehofer et al Am J Transpl 2013;13:253-265

AS and NAS after OLTx

A team Approach including:

�Hepatologists

�Endoscopists

�Transplant Surgeons

�Interventional radiologists

Results in the most effective and efficient treatmentapproach for these patients


2010:ulteriori episodi febbrili a cadenza quasi mensile, trattate con terapie antibiotiche empiriche e mirate(a seconda della presenza o meno di isolati)

2011:Colangio-RM: stenosi moderata dell’anastomosi biliareEseguita colangiografia percutanea (PTC) complicatada sepsi da E. coli ESBL-produttore


2012-2013:ulteriori ricoveri e trattamenti antibiotici, sia empirici che mirati (ertapenem e.v.)

2014:non più episodi settici in regime di ricovero

Quali prospettive x questo paziente?

Profilassi antibiotica(antibiotici a dose ridotta)

Atresia delle VB

Stenosi post-chirurgiche

- coledoco-duodenostomia - coledoco-digiunostomia - ricostruzione delle vie biliari

Infezioni ascendenti croniche

1. controllare carica batterica biliare

2. ridurre le recidive

Terapia orale (dosi ridotte)per circa 3 mesi

Westphal J-F and Brogard JM, Drugs 1999 Jan; 57 (1): 81-91

Conclusione 2:infezioni ricorrenti delle vie biliari (1999)

Conclusione 2:infezioni ricorrenti delle vie biliari (2014)

Non profilassi ma terapia cronicao terapia mirata delle batteriemie

Si cerca di impedire lo sviluppo di ceppi produttori di ESBLo CRE

Causa anatomica non rimovibile+

Terapia orale inefficace

Decontaminazione intestinale?Fecal transplantation (x i colonizzati da CRE)?

Azienda Ospedaliera Papa Giovanni 23° - Bergamo · PDF fileAzienda Ospedaliera Papa...

Documents

Transcript of Azienda Ospedaliera Papa Giovanni 23° - Bergamo · PDF fileAzienda Ospedaliera Papa...