Azienda Ospedaliera
Papa Giovanni 23° - Bergamo
Fondazione per la Ricerca Ospedale Maggiore di Bergamo - FROM
Le infezioni delle vie biliari
A 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
Caso clinico 1:
febbre e addominalgie
All’ecografia addome: marcata
idrope della colecisti
con pareti nettamente ispessite
(fino a 1 cm) contenente
un calcolo infudibolare di 2-3 cm
… non dilatazione VB …
VALUTAZIONE CHIRURGICA
La storia
“In conclusion I wish to express the hope that some day
surgeons will be fairly unanimous in their views on the
treatment of acute inflammations of the gall-bladder.”
Ann Sur. 1928
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 primo
episodio (Badia 2014)
Materiali e metodi
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
Risultati
502 pazienti
62.09 anni
56.2% maschi
Charlson’s comorbidity index 3
Risultati per trattamento
p<0.0001
p<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
-431 €
+751 €
Analisi del timing operatorio early
p<0.0001
p<0.0001
p=NS
p=NS
Risultati per periodo
2 periodi individuati 01/1/08-31/5/10 e 1/6/10 -30/4/13
Gruppi omogenei per caratteristiche demografiche
Risultati per periodo
p<0.043
p<0.0001
Risultati per periodo early
p=NS
p=NS
ACC: Colecistite Acuta Calcolosa
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
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 DIAGNOSIS
A) 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
Abdominal
Ultrasound
•Biliary stones/sludge
•Wall thickness: =5mm
•Fluid collection around
cholecystitis
•Ultrasound Murphy
If possible obtain stones
size(=5mm)
1
ACC?
CONFERMA di SOSPETTO di CALCOLOSI DELLA VIA
2
BILIARE PRINCIPALE
Sospetti
Fattori Predittivi di Coledocolitiasi
MOLTO FORTI
FORTI
MODERATI
CVBP evidenziati all’ecografia transaddominale
Colangite ascendente
Bilirubina > 4
Calcoli via
biliare
?
Coledoco > 6 mm (con colecisti in sede)
Bilirubina tra 1.8 e 4
Anormalità dei test epatici differenti dalla Bilirubina
Età>55 aa
Pancreatite biliare
Classi di Rischio per Coledocolitiasi
ALTA
Presenza di uno dei “FATTORI PREDDITIVI MOLTO FORTI”
ERCP
Oppure
Presenza di entrambi “FATTORI PREDITTIVI FORTI”
BASSA
Assenza di FATTORI PREDITTIVI
INTERMEDIA
TUTTI GLI ALTRI CASI
NIENTE
Ecoendo
vs.
Colangio RM
QUALE TRATTAMENTO PER LA LITIASI VIA BILIARE
IN COLECISTITE CALCOLOSA?
3
Candidato a
Intervento?
http://www.triveneta.org/slides/Trieste240911/02
-roseano.pdf
CUT-OFF DI MORTALITA’ 10%
3
Candidato a
Intervento?
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?
NO
Risorse Umane/Strumenti:
Chirurgo-Anestesista Sala Operatoria
H24 (Strumenti: P-Possum Score
http://berian.altervista.org/portale/ppos
sum/ , Giudizio Clinico)
Disponibilità attuale: Sì
Risorse aggiuntive: NO
Pronto Soccorso/
Medicina Urgenza/
Gastro2
3
Candidato a
Intervento?
NO
ANTIBIOTICO
PER 48 ORE
FALLIMENTO
ATB?
S
I
Risorse Umane/Strumenti:
Medico-Infermiere Med Urg; MedicoInfermiere Gastro 2; Radiologo Interventista
(Strumenti: Antibiotici, Ecografia
interventistica)
Disponibilità attuale: Sì
Risorse aggiuntive: NO
COLECISTOSTOMI
A
Medicina Urgenza/
Gastroenterologia 2
3
Candidato a
Intervento?
NO
ANTIBIOTICO
PER 48 ORE
FALLIMENTO
ATB?
SI
COLECISTOSTOMIA
FALLIMENTO
COLECISTOSTOMIA?
INTERVENTO
Risorse Umane/Strumenti:
Medico-Infermiere Med Urg; Medico-Infermiere
Gastro 2; Radiologo Interventista, ChirurgoInfermiere Chir 1; Anestesista-Personale Sala H24
(Strumenti: Antibiotici, Ecografia interventistica, Sala
Operatoria H24)
Disponibilità attuale: Sì
Risorse aggiuntive: NO
Medicina Urgenza/
Gastroenterologia 2/
Chir 1
Colecistite
Via Biliare
Selezione Paziente
Colecistite + VBP-:
•Candidato ad intervento: Intervento urgenza differibile (Gestione Chirurgia 1)
•Non candidato ad intervento: Antibiotico, eventuale colecistostomia (Gestione Medicina
d’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 (Gestione
Gastroenterologia 2; eventuale intervento se colecistostomia inefficace)
Caso clinico 1:
febbre e addominalgie
La paziente non ha indicazioni chirurgiche
ha già eseguito emocolture
Quale terapia antibiotica empirica?
Tempestiva
Corretta
Ottimizzata
Tokyo Guidelines 2013
for 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
Quale dose ?
- dose carico antibiotici
- dose di mantenimento
Considerare i focolai eradicabili
Isolamenti microbiologici da bile
e sangue nelle infezioni acute biliari
Isolati
bile %
sangue %
Gram negativi
Escherichia coli
Klebsiella spp
Pseudomonas spp
Enterobacter spp
31-44
9-20
0,5-19
5-9
35-62
12-28
4-14
2-7
3-34
9-20
4-20
10-23
6-9
1
Gram positivi
Enterococcus spp
Streptococcus spp
Anaerobi
J. Hepatobiliary Pancreat Sci (2013) 20: 60-70
Antibiotici ad elevata
concentrazione biliare/colecistica
Penicilline
Cefalosporine
1° gener.
2° gener.
3° gener.
Ampicillina, piperacillina, pipera/tazo
Cefazolina
Cefmetazolo, cefotiam
Cefoperazone/sulbactam, ceftriaxone,
ceftazidime
Fluorchinoloni
Ciprofloxacina
Monobattami
Aztreonam
Carbapenemi
Meropenem
Lincosamidi
Clindamicina
Gicilcicline
Tigeciclina
Hepatogastroenterology 1996; 43: 800-6
E’ necessario utilizzarli?
Non è strettamente indispensabile
L’escrezione antibiotica biliare si ferma
se vi è ostruzione biliare
La terapia può fallire se non è associata
alla disostruzione delle VB
Van den Hazel, CID1994 Aug;19(2):279-86, WSES Guidelines 2013, TG 2013
Terapia antibiotica empirica delle
colecistiti/colangiti: il protocollo aziendale
COMUNITARIA
OSPEDALIERA
ESBL -
ESBL +
No sepsi
grave
Sepsi grave
Amoxi
/clav
Pip/ta
zo
Cipr
o+
metr
o
No sepsi
grave
Pip +
Tige
+/Fluco
Se allergia
Tige
ciclin
a
Adattato da WSES Guidelines 2013, TG 2013
Sepsi grave
Mero(ImiDori)
+/Vanco
+
Echino
OO.RR.BG/HPG23:
bacilli G-isolati da bile – 2012/14
34 isolati positivi di cui
5 ESBL produttori
9
15
(14,7%)
3/34 produttori
di carbapenemasi
10
E. coli
K. Pneumoniae
Altri
(8,8%)
Microbiologia HPG23: dati dal 1/1/2012 al 31/03/2014
Come identificare i pz a rischio x ESBL?
Attribute
No. of points
Recent antibiotic therapy with beta-lactams a
and/or fluorquinolones
Previous ospitalization
b
2
3
Transfer from another healthcare facility
3
Charlson comobidirty score > 4
2
Recent history of urinary catheterization c
2
Age > 70 years
2
a
b
c
During the 3 months preceding the index hospitalization
During the 12 months preceding the index hospitalization
During the 30 days preceding the index hospitalization
Tumbarello M. et al.: Antimicrob. Agents Chemother. July 2011, 3485-3490
Come identificare i pz a rischio x
ESBL?
Score ≥ 3: ESBL carrier possible
Start with tigecicline or carbapenem then shift if not
confermed
Score ≥ 8: ESBL high probable
Start with tigecicline or carbapenem.
The patient should be isolated.
Tumbarello M. et al.: Antimicrob. Agents Chemother. July 2011, 3485-3490
Jhonson SW. Et al: Infect Control Hosp Epidemiol 2013 April; 34(4): 385-392
Durata della terapia antibiotica:
da WSES 2013 e TG 2013
Se colecistectomia:
stop terapia dopo 24 ore dall’intervento
Se la fonte di infezione è controllata:
4-7 gg
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 con
piperacillina/tazobactam
4,5 g in SF 100 cc x 3/die
Miglioramento
clinico
Miglioramento
ecografico
Dimessa in riabilitazione
(16 gg di degenza)
Conclusione 1:
infezione acuta delle vie biliari
Scopo del trattamento è bonificare il sito di infezione
Disostruzione
Terapia antibiotica
- tempestiva
- corretta
- ottimizzata
+
(se stasi l’antibiotico
non viene escreto
nelle VB)
Westphal J-F and Brogard JM, Drugs 1999 Jan; 57 (1): 81-91
Caso clinico 2:
colangiti febbrili recidivanti
Paziente VL, uomo, 63 anni
16/02/2009: OLTx per cirrosi HBV-HDV correlata
Anastomosi bilio-biliare T-T
Immunosoppressione: FK + steroide
Maggio 2009: indici di colestasi elevati
All’ERCP: stenosi serrata dell’anastomosi a livello del dotto epatico
comune, sfinterotomia, dilatazione pneumatica e posizionamento
di endoprotesi biliare
Caso clinico 2:
colangiti febbrili recidivanti
Giugno 2009: nuovo ricovero per
colangite.
Rimossa per via endoscopica la protesi
biliare (non ostruzione)
Caso clinico 2:
colangiti febbrili recidivanti
26/08/2009: nuovo ricovero per febbre,
all’ERCP stenosi serrata dell’anastomosi
+ coledocolitiasi della VB preanastomotica
Caso clinico 2:
colangiti febbrili recidivanti
30/11/2009: all’ERCP rimossa
endoprotesi biliare precedente,
posizionata
doppia endoprotesi
Caso clinico 2:
colangiti febbrili recidivanti
Persistenza di episodi febbrili
da enterobatteri
Gennaio 2010
Confezionamento di anastomosi
bilio-digestiva su ansa Y
presso la Chirurgia 3
Acute Cholangitis: Definition
Acute Cholangitis: A morbid condition with acute
inflammation and infection in the bile ducts. It results from
a combination of biliary obstruction and bacterial growth in
the 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 in
maintaining the sterility of bile.
Bile salts have bacteriostatic properties.
The sphincter of Oddi controls the direction of bile flow and serves as a
barrier 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 less
frequently 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 allowing
translocation of bacteria or endotoxin into the vascular and
lymphatic system (cholangio-venous/lymphatic reflux)
Translocation of bacteria into the bloodstream results in
septicemia, 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 clinical
cholangitis.
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 and
intestine.
Patients with incomplete biliary obstruction have been shown to have a
higher 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 always
present in patients with acute cholangitis, and further diagnostic
testing may be required before the diagnosis can be established.
Fever and abdominal pain
Jaundice
Shock and altered mental status
80%
60-70%
3,5-7%
Acute Cholangitis: Diagnostic Criteria
Standard diagnostic criteria for acute cholangitis have been
lacking, and various definitions for the disease have been used
in the past.
The “Tokyo Guidelines” recently recommended a more
systematic approach, using a combination of clinical features,
laboratory data, and imaging findings to diagnose acute
cholangitis.
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 directed
toward the two main etiologic components of
the disease:
Biliary infection
?
Systemic antibiotics
Biliary obstruction ?
Biliary drainage
Appropriate supportive care
Acute Cholangitis:Therapeutic Management
Biliary Drainage
ERCP +ES + PS or SEMS placement
PTBD
Trans-duodenal papillo-sphincterotomy/sphincteroplasty
Roux en Y Hepaticojejunostomy
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 clinical
implications for OLTx
Bile ducts are supplied only arterially.
Biliary epithelium is more liable to ischemic injury
than hepatocytes.
Severe hypotension eventually leads to an “ischemic
cholangiopathy” 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, without
effective passage of contrast material, as identified by
cholangiography. They result mainly from surgical technique and
local ischemia, leading to fibrotic scarring of the anastomosis.
They
involve
choledocho-choledochostomy
or
choledochojejunostomy. 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 control
in both donor and recipient.
Tension of the duct anastomosis.
Small bile leaks resulting in a peri-anastomotic fibroinflammatory response.
Ischemia at the end of the bile duct resulting in fibroproliferative 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
Anastomotic Strictures (AS): Therapy
ERCP balloon dilatation and plastic stent placement
ERCP balloon dilatation and full covered expandable
metal stent placement
PTC + external/internal biliary drainage ±
expandable metal stent placement
Roux en Y hepatico-jejunostomy
OLTx within 3 months or more than 5mg of
prednisone per day:
Dilation with a 10F biliary dilator, and a 10 F
stent placed for 12 weeks
During a subsequent ERCP. The stent was
removed and balloon dilation was performed
with a balloon (6-10 mm diameter) for 1
minute.
A sphincterotomy was performed with the
standard technique and a maximal number (up
to 9) of 8,5F to 11,5F stents were placed across
the anastomosis
OLTx more than 3 months and less than 5mg
of prednisone per day:
Initial ERCP with 1 minute balloon dilation
followed by placement of the maximal number
of stents at the initial and subsequent ERCP
Follow up:
Liver function tests and clinical evaluation
every 12 weeks
Only 1 or 2 stents in place ?
ERCP at 3
months intervals or earlier if signs or symptoms
of biliary obstruction
3 or more stents in place ?
ERCP and stent
exchange only when signs or symptoms of
biliary obstruction or after 1 year without stent
exchange, whichever came first
Group A: PCMS Partially Covered Metal Stent diameter 10 mm Length 60,80,100 mm
Group B: FCfins Fully covered with fins; diameter 10 mm, length 40,60,80,100 mm
Group 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 a
single PS) and easy removal.
Both strategies have very high technical success rates and low adverse event
rates in ABSs of OLT patients, despite the need for multiple ERCPs per
patient.
A much lower stent migration rate with MPS compared with a single PS and
covered SEMS have been reported
MPSs with a minimal stent duration of 12 months and CSEMS with a minimal
stent duration of 3 months had similar ABS resolution rates after OLTx
Current evidence does not suggest a clear advantage of SEMS use over MPSs
in 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 MPSs
has failed ?
•Is an SEMS duration as long as 6 months safe and feasible, and can it replace
multiple 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 further
clarification
Non Anastomotic Biliary Strictures (NAS)
Definition: NAS are strictures at any location in the biliary
system of the transplanted liver (intrahepatic or extrahepatic).
First described after OLTx as a cholangiographic image of biliary
strictures and dilatations caused by ischemia after HAT.
However, such cholangiographic abnormalities of strictures and
dilatations can also be seen in patients who do not have HAT
and 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 for
oxygenation
Cholangiocytes are highly susceptible to reoxygenation after
anoxia (reperfusion injury)
In DCD warm ischemia time in the donor in addition to
subsequent cold-ischemia reperfusion injury is believed to
result 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 the
development of NAS
Transplantation 2011;92:373-379
Non Anastomotic Biliary Strictures (NAS)
Zone A: Hilar bifurcation
Zone B: Ducts between the first- and second- order branches
Zone C: Ducts between the second-and third- order branches
Zone D: Periphery of the liver
Anastomotic
BiliaryStrictures
Strictures (NAS)
(NAS)
Non Non
Anastomotic
Biliary
Early (< 1 year)
Location: bile duct
bifurcation and extrahepatic
bile duct.
Late (> 1 year)
Location: more frequently in
the periphery of the liver.
Mechanism: Ischemia
mediated (longer cold and
warm ischemia)
Mechanism: Immunemediated
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 perfusion
pressure of preservation
solution
Cytotoxic effect of
hydrophobic 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 treatment
approach 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 biliare
Eseguita colangiografia percutanea (PTC) complicata
da 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?
Conclusione 2:
infezioni ricorrenti delle vie biliari (1999)
Profilassi antibiotica
(antibiotici a dose ridotta)
Atresia delle VB
1. controllare carica
batterica biliare
2. ridurre le recidive
Stenosi post-chirurgiche
- coledoco-duodenostomia
- coledoco-digiunostomia
- ricostruzione delle vie biliari
Terapia orale
(dosi ridotte)
per circa 3 mesi
Infezioni ascendenti croniche
Westphal J-F and Brogard JM, Drugs 1999 Jan; 57 (1): 81-91
Conclusione 2:
infezioni ricorrenti delle vie biliari (2014)
Causa anatomica non rimovibile
+
Terapia orale inefficace
Non profilassi ma terapia cronica
o terapia mirata delle batteriemie
Si cerca di impedire
lo sviluppo di ceppi
produttori di ESBL
o CRE
Decontaminazione intestinale?
Fecal transplantation (x i colonizzati da CRE)?