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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
Risultati per trattamento
•1,03 vs 2,13 accessi in ospedale
•Guadagno di 5,3 giorni di degenza
•2263 € risparmio per la struttura
•Non complicanze aggiuntive
Risultati per trattamento
+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
Risorse Umane/Strumenti:
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
Risorse Umane/Strumenti:
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)
Caso clinico 1:febbre e addominalgie
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,
Caso clinico 1:febbre e addominalgie
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
Caso clinico 2:colangiti febbrili recidivanti
Giugno 2009: nuovo ricovero percolangite.
Rimossa per via endoscopica la protesibiliare (non ostruzione)
Caso clinico 2:colangiti febbrili recidivanti
26/08/2009: nuovo ricovero per febbre,all’ERCP stenosi serrata dell’anastomosi
+ coledocolitiasi della VB pre-anastomotica
Caso clinico 2:colangiti febbrili recidivanti
30/11/2009: all’ERCP rimossaendoprotesi biliare precedente,
posizionatadoppia endoprotesi
Caso clinico 2:colangiti febbrili recidivanti
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
Acute Cholangitis: Pathophysiology
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
Acute Cholangitis: Pathophysiology
� 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
Gastrointestinal Endoscopy, 2013;77(5):679-691
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
Gastrointestinal Endoscopy, 2013;77(5):679-691
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
Non Anastomotic Biliary Strictures (NAS)
� 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
Non Anastomotic Biliary Strictures (NAS)
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
Non Anastomotic Biliary Strictures (NAS)
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
Non Anastomotic Biliary Strictures (NAS)
Non Anastomotic Biliary Strictures (NAS)
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
Caso clinico 2:colangiti febbrili recidivanti
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
Caso clinico 2:colangiti febbrili recidivanti
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)?