Beneficial role of terlipressin in
decompensated cirrhotics with spontaneous
bacterial peritonitis
Alberto Ferrarese
a
, Valerie Tikhonoff
b
, Edoardo Casiglia
b
, Patrizia Burra
a
and
Marco Senzolo
a
,
a
Multivisceral Transplant Unit, Department of Surgery, Oncology
and Gastroenterology and
b
Department of Medicine, Padua University Hospital,
Padua, Italy
Correspondence to Marco Senzolo, MD, PhD, Multivisceral Transplant Unit,
Department of Surgery, Oncology and Gastroenterology, Padua University
Hospital, Padua 35100, Italy
Tel: + 39 049 821 8726; fax: + 39 049 821 8727;
e-mail: marcosenzolo@hotmail.com
Received 6 October 2016 Accepted 10 October 2016
We have read with interest the manuscript by Salman et al.
[1], who investigated different therapeutic approaches to
treat spontaneous bacterial peritonitis (SBP) in patients
with cirrhosis. The authors evaluated haemodynamic
changes during SBP, showing an increase in cardiac output
(CO) and a contemporary decrease in systemic vascular
resistances (SVRs), 3 days after starting conventional
therapy ( + 16.2 ± 10.3 and - 8.9 ± 9.9%, respectively). In
this group, 2/50 patients did not recover from SBP; in
addition, novel therapeutic approaches failed to increase
survival, even though the use of terlipressin significantly
improved haemodynamics.
During SBP, several other factors can affect haemody-
namics, such as the need for large volume paracentesis (LVP),
which can further deteriorate this equilibrium. We evaluated
intra-individual haemodynamic changes before and after
resolution of nosocomial SBP in a 58-year-old patient admit-
ted to our ward for end-stage alcoholic liver disease, while
undergoing LVP. Before infection, LVP determined a
21% decrease of SVR in respect of baseline values
(1857.5–1468.2 dyn × s/cm
5
), with a contemporary slight
increase in CO (3.9–4.0 l/min). In contrast, while LVP was
performed during an episode of SBP, a signi ficantly greater
decrease in SVR (675.9–464.5 dyn × s/cm
5
, - 31.2%) was
noted; consequently, CO was increased at baseline in com-
parison with the first LVP and there was a further increase
after LVP (9.85–12.9 l/min) to counterbalance systemic vaso-
dilation. During the third LVP, after SBP resolution, haemo-
dynamics was similar to the values before infection (Fig. 1).
This confirms the findings of the authors and in parti-
cular the need for a preserved cardiac function to effec-
tively increase CO and to counterbalance the lowering of
SVR during LVP. In addition, our case showed a further
decrease in SVR (- 50%) during sepsis. Thus, terlipressin
introduction, which has been associated with a significant
increase in SVR by 61% [2], may reduce the risk of renal
impairment in these patients.
Because of the published evidences that β-blockers could
worsen the prognosis of decompensated cirrhosis [3,4], in
particular, during infection [5], withdrawal of NSBB has been
recommended. However, in the present study, mortality
because of variceal bleeding was 9/200 (4.5%) and it is not
known whether β-blockers were withdrawn after SBP.
Furthermore, it could be interesting to evaluate whether the
incidence of variceal bleeding was lower in the terlipressin
groups.
Therefore, even though in this study survival was not
significantly different between groups, terlipressin could be
considered an option in cirrhotics with SBP undergoing
LVP or with impaired cardiac function or high-risk varices
when withdrawal of β-blockers is recommended.
Acknowledgements
Conflicts of interest
There are no conflicts of interest.
References
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therapeutic modalities on systemic, renal, and hepatic hemodynamics and
short-term outcomes in cirrhotic patients with spontaneous bacterial perito-
nitis. Eur J Gastroenterol Hepatol 2016; 28:777–785.
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3 Ge PS, Runyon BA. The changing role of beta-blocker therapy in patients
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DOI: 10.1097/MEG.0000000000000797
Systemic vascular resistances, dyn.s.cm
−5
Cardiac Output, l/m
2.5
Pre Post
30.9%
Pre Post
20.9%
6.4%
31.2%
(a)
(b)
Fig. 1. Haemodynamic changes before and after three consecutive large
volume paracentesis. (a) Systemic vascular resistances; (b) cardiac output.
European Journal of Gastroenterology & Hepatology 2017, 29:366
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