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Managing Local Complications
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66. Varadarajulu S, Noone TC, Tutuian R, Hawes RH,
Cotton PB.Predictors of outcome in pancreatic duct
disruption managed by endoscopic transpapillary stent
placement. Gastrointest Endosc. 2005;61(4):568–75.
https://doi.org/10.1016/s0016- 5107(04)02832- 9.
67. Verma S, Rana SS.Disconnected pancreatic duct syndrome: updated review on clinical implications and
management. Pancreatology. 2020;20(6):1035–44.
https://doi.org/10.1016/j.pan.2020.07.402.
68. Irani S, Gluck M, Ross A, et al. Resolving external pancreatic stulas in patients with disconnected
pancreatic duct syndrome: using rendezvous techniques to avoid surgery (with video). Gastrointest
Endosc. 2012;76(3):583–6. https://doi.org/10.1016/j.
gie.2012.05.006.
69. Kochhar R, Jain K, Gupta V, etal. Fistulization in the
GI tract in acute pancreatitis. Gastrointest Endosc.
2012;75(2):436–40. https://doi.org/10.1016/j.
gie.2011.09.032.
70. Ho HS. Gastrointestinal and pancreatic complications associated with severe pancreatitis. Arch Surg.
1995;130(8):817. https://doi.org/10.1001/arch-
surg.1995.01430080019002.
71. Jiang W, Tong Z, Yang D, et al. Gastrointestinal
stulas in acute pancreatitis with infected pancreatic or peripancreatic necrosis. Medicine (Baltimore). 2016;95(14):e3318. https://doi.org/10.1097/
MD.0000000000003318.
72. Timmerhuis HC, Van Dijk SM, Hollemans RA, etal.
Perforation and stula of the gastrointestinal tract in
patients with necrotizing pancreatitis: a nationwide
prospective cohort. Ann Surg. 2023;278(2):e284–92.
https://doi.org/10.1097/SLA.0000000000005624.
73. Sikora SS, Khare R, Srikanth G, Kumar A, Saxena
R, Kapoor VK.External pancreatic stula as a sequel
to management of acute severe necrotizing pancreatitis. Dig Surg. 2005;22(6):446–52. https://doi.
org/10.1159/000091448.
74. Al-Diery H, Phillips A, Evennett N, Pandanaboyana S, Gilham M, Windsor JA. The pathogenesis of nonocclusive mesenteric ischemia:
implications for research and clinical practice. J
Intensive Care Med. 2019;34(10):771–81. https://doi.
org/10.1177/0885066618788827.
75. Sissingh NJ, Groen JV, Koole D, et al. Therapeutic
anticoagulation for splanchnic vein thrombosis in
acute pancreatitis: a systematic review and metaanalysis. Pancreatology. 2022;22(2):235–43. https://
doi.org/10.1016/j.pan.2021.12.008.
76. Szatmary P, Grammatikopoulos T, Cai W, et al.
Acute pancreatitis: diagnosis and treatment. Drugs.
2022;82(12):1251–76. https://doi.org/10.1007/
s40265- 022- 01766- 4.
77. van Brunschot S, van Grinsven J, Voermans RP,
etal. Transluminal endoscopic step-up approach versus minimally invasive surgical step-up approach in
patients with infected necrotising pancreatitis (TENSION trial): design and rationale of a randomised
controlled multicenter trial [ISRCTN09186711].
BMC Gastroenterol. 2013;13(1):161. https://doi.
org/10.1186/1471- 230X- 13- 161.
Managing Organ Failure inAcute
https://t.me/med1917
Pancreatitis
LuKe, WenjianMao, andWeiqinLi
Key Points
1. The presence and duration of organ failure
determine the severity and classication of
acute pancreatitis.
2. Organ failure is preceded by organ dysfunction, and this can occur in a single organ system or as multiple organ dysfunction
syndrome (MODS).
3. Important systemic contributors to organ failure include inammation, microcirculatory
dysfunction, and coagulopathy.
4. Additional factors contribute to different
organ failure, for instance, respiratory
(increased intra-abdominal pressure and
restricted diaphragmatic excursion), renal
(hypovolemia), cardiovascular (hypovolemia
and distributive shock), and intestinal (ischemia and iatrogenic factors).
5. Each organ system requires specic management, including ventilation, dialysis, inotropes, and enteral nutrition, respectively.
L. Ke · W. Li (*)
Department of Critical Care Medicine, Jinling
Hospital, Medical School of Nanjing University,
Nanjing, Jiangsu, China
National Institute of Healthcare Data Science,
Nanjing University, Nanjing, Jiangsu, China
e-mail: ctgkelu@nju.edu.cn
W. Mao
Department of Critical Care Medicine, Jinling
Hospital, Medical School of Nanjing University,
Nanjing, Jiangsu, China
1 Introduction
Organ failure (OF) is the key determinant of mortality in patients with acute pancreatitis (AP) and
is the key criterion for grading the severity of AP
[1, 2]. Previously, it was considered that OF and
infected pancreatic necrosis (IPN) were equivalent determinants of mortality [3], but there has
been considerable progress in the management of
IPN, including drainage-rst strategy and a step up approach to laparoscopic and endoscopic
necrosectomy [4, 5]. This has resulted in a
decreased incidence of new-onset OF and mortality compared with open surgical necrosectomy,
which means that OF is the most important determinant of severity and mortality, while IPN is
still associated with increased morbidity but it
has less impact on mortality [6].
Organ failure is preceded by organ dysfunction
and can involve single or multiple organ systems.
Most patients with OF require intensive care unit
(ICU) admission, leading to considerable utilization of healthcare resources. Failure of different
organ systems are not equivalent in terms of prognosis. The outcome is worse with multiple (rather
than single) OF [6], longer duration OF [7], and
certain combinations of individual OFs [8].
The genesis of OF during AP was previously attributed to acinar cell-initiated cytokinemediated systemic inammation and the release
of activated digestive enzymes [9]. Over the last
two decades, there have been important discoveries that have provided new insights into the
© The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2024
J. A. Windsor et al. (eds.), Acute Pancreatitis, https://doi.org/10.1007/978-981-97-3132-9_17
235
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L. Ke et al.
pathophysiology and evolution of OF. These
include increased capillary permeability (with
tissue and organ edema) [10], reex splanchnic
vasoconstriction with impaired organ perfusion
(including kidneys, pancreas, and intestine) [11],
and extensive coagulopathy [12] and lipotoxicity
(Chap. 6). These factors all contribute to the development of OF and have implications for management strategies. Newer concepts, including the
gut-lymph model of organ failure, will likely result
in new specic treatment strategies [13].
The management of AP requires accurate prediction of severe AP (i.e., persistent OF, lasting
>48 h), monitoring of the clinical course, and
denition of severity, which vary among studies
[14–16]. The Revised Atlanta Classication
(RAC) [1] recommends the modied Marshall
scoring system to be used to dene the severity of
AP, but this is not entirely suitable for patients in
ICU because it does not take into account the
need for mechanical ventilation and the importance of different doses of inotropes or include
the intestine as an organ that not only fails but
also contributes to the severity of OF.The preference is to use the Sequential Organ Failure
Assessment (SOFA) score, especially for critically ill AP patients [17].
The aim of this chapter is to provide a practical guide to the intensive care management of the
most common types of OF in severe AP.
2 Prediction ofPersistent
Organ Failure
When treating a patient with initial/mild organ
dysfunction in the ward/emergency room, it is
crucial to identify those at high risk of developing
persistent OF to ensure timely ICU admission.
There are several diagnostic tools available in
clinical practice. Mounzer et al. compared a
series of clinical scoring systems for predicting
persistent OF and found that all the conventional
scores for AP prognosis assessment, including
the Ranson score, APACHE II score, and BISAP
score, had only modest sensitivity and overall
predictive performance [18].
Apart from these commonly used scoring systems in AP, the quick Sequential Organ Failure
Assessment (qSOFA) score, developed for rapid
identication of patients with suspected infection
outside ICU, consists of only three items: respiratory rate, altered mentation, and systolic blood
pressure [19]. Rasch etal. tested the qSOFA score
in a cohort of 203 AP patients in the emergency
room and found it has moderate accuracy in predicting ICU admission with an area under the
curve (AUC) of 0.73 [20]. The authors also developed a new scoring system called the emergency
room assessment of acute pancreatitis (ERAP)
score by adding two rapidly available laboratory
parameters: blood urea nitrogen and C-reactive
protein (CRP). The ERAP score, compared with
the original qSOFA, increases the AUC in predicting ICU admission to approximately 0.79. In a
large cohort of more than 2000 patients, Shi etal.
developed a nomogram to predict persistent OF,
consisting of 6 items: age, respiratory rate, albumin, lactate dehydrogenase, oxygen support, and
pleural effusion [21]. The nomogram demonstrates an AUC of 0.814 in external validation,
although it is more complex to use, requiring laboratory data and additional examination. The
advent of articial intelligence has resulted in the
application of machine learning algorithms to the
prediction of AP severity, including organ failure.
This approach results in improved predictive
validity and accuracy and is covered in Chap. 8.
Taken together, repeated clinical assessment
should be carried out when treating early AP
patients in the ward/emergency room since all the
available scoring systems have only modest accuracy. Special attention should be paid when the
patients show increased respiratory rate or signicantly altered laboratory measures like CRP.
3 Management ofAcute
Respiratory Failure
Respiratory failure is the most common type of
OF in AP patients [14]. A recent cohort study
found that respiratory failure occurred in 92% of
acute necrotizing pancreatitis patients with OF,
and the incidence peaked during the rst week.
Of the three most frequently affected organ systems (respiratory, renal, and cardiovascular),
the respiratory system was the rst to fail and
Managing Organ Failure inAcute Pancreatitis
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237
persisted for the longest time [14]. In a large
cohort study involving more than 800,000 hospitalized AP patients, Gajendran etal. found that
5.4% of AP patients developed respiratory failure, with a mortality rate of 26.5%. Important
predictors of respiratory failure were pleural
effusion and pneumonia, and the presence of
respiratory failure signicantly increased hospital stay and risk of mortality [22]. For the occurrence of persistent respiratory failure, Li et al.
developed a simplied Lung Injury Prediction
Score (sLIPS) incorporating oxygen requirement, hypoalbuminemia, and obesity. They demonstrated that sLIPS could accurately predict
persistent respiratory failure with an AUC of
0.81in an external validation cohort [23].
3.1 Oxygen Therapy
Hypoxemia is common in AP mainly because of
ventilation/perfusion (V/Q) mismatch. In this
regard, the UK guidelines recommended that
oxygen supplementation be provided to patients
with a diagnosis of AP regardless of severity in
2005 [24]. Since there is no additional evidence
either for or against this recommendation in
recent years, it has been practiced variably worldwide. Oxygen therapy can be implemented
through nasal prongs or a face mask. In recent
years, non-invasive high-ow oxygen therapy has
attracted signicant attention as a bridge between
simple oxygen supplementation and mechanical
ventilation (i.e., to delay or avoid the need for
this) [25]. In a small cohort study involving 69
patients with AP-associated respiratory failure,
the use of high-ow oxygen therapy, compared to
conventional oxygen therapy, was associated
with a lower intubation rate and shortened intensive care unit stay [26]. The clinical value of
high- ow oxygen therapy should be assessed in
future prospective trials.
3.2 Anti-Inammatory Therapy
Since AP is an inammatory disease by its nature,
the use of anti-inammatory therapy makes
sense. In severe cases of AP, local injury and
inammation in the pancreas proceeds to systemic inammation (see Chap. 5). Plateletactivating factor (PAF) is an important
inammatory mediator, recruiting white cells
into inammatory sites. Animal studies showed
that PAF participated in the progression of AP by
activating the interleukin system in endothelial
cells and promoting tissue damage in multiple
organs, including the lung [27]. Lexipafant,
which is a PAF inhibitor, was tested in AP patients
in the hope of reducing the incidence of organ
failure. However, the multicenter, double-blind,
phase III trial conducted in patients with predicted severe acute pancreatitis failed to show
benet from lexipafant therapy in preventing any
type of new organ failure [28]. However, the evidence did show clinical benet if PAF was
administered within 48h of admission [29], but
this has not been conrmed in a subsequent adequately powered randomized controlled trial.
Despite multiple trials evaluating a range of antiinammatory therapies, there are no evidencebased recommendations in management
guidelines for anti-inammatory or other specic
treatments for AP [30]. There is now evidence of
the equivalence of non-steroidal anti-inammatory medication and opioids in treating pain, at
least in patients with non-severe AP (see Chap.9),
but an impact on organ failure incidence and
severity has not been demonstrated.
3.3 Mechanical Ventilation
Mechanical ventilation is a lifesaving treatment
for patients with severe respiratory failure. In
patients with AP-related respiratory failure, it is
noteworthy that intra-abdominal hypertension
(IAH), which is relatively common in severe AP
[31], is a vital contributor to the underlying
pathophysiology, which must be considered
when implementing mechanical ventilation in
this cohort. Pelosi et al. described the effect of
IAH on respiratory mechanics using obese
patients as the study group [32] and found that
increased intra- abdominal pressure (IAP) led to
increased chest wall elastance (impaired compli-
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L. Ke et al.
ance), consequently reducing lung volume and
promoting atelectasis formation. In a physiological animal model incorporating AP and IAH, the
addition of 20 or 30 mmHg resulted in signicantly dropped arterial PO2 and decreased venous
oxygen saturation, suggesting impaired tissue
oxygen delivery [33]. Given the unique pathophysiology of respiratory failure in AP, the management strategy of acute respiratory failure in
AP is technically different from that used in
patients with acute respiratory distress syndrome
(ARDS), although the underlying philosophy is
the same: maintain adequate oxygenation and
ventilation while protecting the lung from unnecessary mechanical injury.
For patients requiring mechanical ventilation
for ARDS, the lung-protective strategy was proposed by ARDSnetwork and widely adopted
worldwide [34]. Back in 2000, a well-designed
and well-conducted large trial conclusively demonstrated the benets of mechanical ventilation
with low tidal volumes in patients with ARDS
Fig. 1 The key
mechanisms for acute
respiratory failure
associated with acute
pancreatitis. Increased
abdominal pressure
leads to a headlong shift
of the diaphragm,
thereby increasing
intrathoracic pressure.
Esophageal pressure can
be seen as a surrogate of
intrathoracic pressure
and used to calculate
trans-pulmonary
pressure
[35]. The clinical benets include reduced mortality and shorter duration of mechanical ventilation. In recently published guidelines, the
recommendation is strong for the lung-protective
strategy, which advocates low tidal volumes
(4–8 mL/kg predicted body weight) and lower
inspiratory pressures (airway plateau pressure≤30cmH2O). However, increased IAP can
lead to cranial shift of the diaphragm, which is
the key and unique extrapancreatic factor contributing to the development of respiratory failure
in AP (Fig.1). Therefore, the mechanical ventilation strategy needs to be modied to address this
issue.
First of all, when considering implementation of
mechanical ventilation in AP patients, IAP should
be routinely measured and at least daily. Moreover,
if available, esophageal pressure, as a surrogate for
intrathoracic pressure, should be measured to calculate trans-pulmonary pressure, which is one of the
main determinants in ventilator-induced lung injury
[36]. For the lung-protective strategy, it is of note
Managing Organ Failure inAcute Pancreatitis
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239
that the recommendation of using an upper limit for
plateau pressures does not take IAP into account.
The fundamental rationale for this recommendation
is to avoid excess trans- pulmonary pressure, which
needs to be reassessed in patients with increased
IAP.When targeting trans-pulmonary plateau pressure at 30 cmH2O, the measured plateau pressure
should be 30cmH2O plus the intrathoracic pressure,
which could be either measured by esophageal
pressure or calculated [37].
3.4 Other Treatments
Because of the role that IAH plays in the pathophysiology of AP-related respiratory failure,
efforts should be made to lower the IAP.Initial
treatment may include reduction in hollowviscera volume like nasogastric drainage, reduction in intra−/extravascular uid content like
restrictive uid therapy (de-escalation, see
Chap. 10), ultraltration or diuretics, and
improvement of abdominal wall compliance,
e.g., adequate analgesia and sedation [38].
Invasive interventions such as percutaneous
catheter drainage (PCD) or even open surgery
should be considered when medical management fails [39]. Moreover, extracorporeal membrane oxygenation (ECMO), a lifesaving
therapy for patients with severe respiratory failure, may be of potential value in the management of AP, though quality studies assessing the
efcacy and safety of ECMO in AP patients are
absent in the literature [40]. More studies are
needed before any formal recommendation can
be made.
4 Management ofAcute Renal
Failure
Acute renal failure or acute kidney injury (AKI)
is common in AP, with varied prevalence in previous reports. In a large, national observational
study, the overall AKI prevalence was 7.9% in
hospitalized AP patients, and it was associated
with poor outcomes. Apart from direct diseaseinduced kidney injury, inappropriate patient
management also plays an important role in AKI
associated with AP.
4.1 Fluid Management
During the acute phase of AP, uid therapy is one
of the mainstay treatments (Chap.10). However,
there are major uncertainties about uid type,
volume, rate, and duration of intravenous uid
[41].
For uid type, there has been an overall consensus that isotonic crystalloid should be the primary choice in the initial treatment of AP, and
Ringer’s lactate is recommended in some guidelines [42]. However, the evidence for this is modest. A recent meta-analysis showed that compared
with saline, Ringer’s lactate did not reduce the
incidence of SIRS, which is supposed to be the
major clinical benet it confers. Still, the studies
were largely small or observational [43]. The
main difference between Ringer’s lactate, other
balanced solutions, and saline lies in their chloride levels. An ongoing large stepped-wedge trial
may provide evidence as to whether the different
chloride levels in different solutions impact
plasma chloride levels sufciently to have a clinically meaningful impact [44]. Current evidence
regarding the effect of different types of crystalloids on clinical outcomes in AP patients is summarized in Table1.
For uid rate, the association between largevolume uid resuscitation and renal complications in AP is not clear due to the lack of
high-quality evidence. An observational study of
179 patients with moderately severe or severe AP
showed that aggressive uid resuscitation (4L or
over in the rst 24 h) was associated with
increased incidence and duration of AKI [45]. In
a recent meta-analysis comparing aggressive
(from 3mL/kg/h to 5mL/kg/h in rst 24h) and
nonaggressive uid strategy in AP, patients
receiving aggressive uid therapy had a higher
rate of AKI [46]. Thus, although early uid resuscitation is indicated for AP patients, excessive
uid administration may be harmful in terms of
causing kidney injury. However, high-quality
evidence is required to draw a rm conclusion.
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There was a signicant
Primary
outcome Main ndings
Prevalence of
Standard
Standard
reduction in SIRS after
24h among subjects
resuscitated with lactated
Ringer’s solution,
compared with normal
saline (84% reduction vs.
0%, respectively;
P=0.035); administration
SIRS at 24h
post-
randomization
resuscitation
with NS
resuscitation
with LR
of lactated Ringer’s
solution also reduced
levels of CRP, compared
with normal saline (51.5
vs. 104mg/dL,
respectively; P=0.02)
Lactated Ringer’s solution
was superior to NS in
SIRS reduction in acute
pancreatitis only in the
rst 24h
SIRS at 48h and mortality
at 24h and 48h
compared to
levels prior to
resuscitation
were not different between
LR and NS
While this trial did not
show a difference in SIRS
prevalence at 24h, LR
prevalence at
24h after
L. Ke et al.
appears to reduce the need
for intensive care and
shortens the length of
hospitalization for acute
pancreatitis
randomization
Study
design n Population Age Group 1 Group 2 Group 3 Group 4
Goal-directed
uid
resuscitation
with NS
uid
resuscitation
with LR
40 AP patients 52.1±19.8years Goal-directed
Multicenter
factorial
RCT
47 AP patients 51.6±17.0years Received NS Received LR SIRS reduction
Single-
center
RCT
42.90±14.05years Received NS Received LR Change in SIRS
patients
121 MAP
Single-
center
RCT
First author
(year),
country
Table 1 RCTs assessing the effect of balanced solution compared to saline on clinical outcomes in acute pancreatitis
Wu etal.
(2011) [84],
USA
Choosakul
etal. (2018)
[85],
Thailand
Lee etal.
(2021) [86],
USA
Managing Organ Failure inAcute Pancreatitis
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The median (p25–p75)
number of SIRS criteria at
48h was 1 (1–2) for NS
vs. 1 (0–1) for LR,
p=0.060. CRP levels
(mg/l) were as follows: At
48h NS 166 (78–281) vs.
LR 28 (3–124), p=0.037;
at 72h NS 217 (59–323)
vs. LR 25 (3–169),
p=0.043
LR inhibited the induction
of inammatory
phenotype of
The number of
SIRS score
levels of CRP at
24h, 48h, and
72h
macrophages and NF-kB
activation
LR was associated with a
reduction in systemic
inammation compared to
NS
Incidence of SIRS at 72h
and occurrence of local
The difference
in CRP level and
SIRS score at
admission and
subsequently
complications were
similar in both groups
Resuscitation with LR is
associated with decreased
severity of AP.It may
derive from how it causes
Measure
systemic
inammatory
response and
lower CRP levels
CRP, pH, and
HCO3 levels
48h after
241
randomization
Received LR
and 1000mL
of 10%
and 1000mL
of 10%
62.54±17.12years Received NS
episode of
AP
40 First
Single-
center
RCT
dextrose
solution
dextrose
solution
Received LR
and 1000mL
of 5%
and 1000mL
of 5%
41.33±14.17years Received NS
48h from
the onset of
51 AP within
Single-
center
RCT
dextrose
solution per
24h
dextrose
solution per
24h
the
symptoms
Received
1000mL of
LR within the
rst hour and
1000mL of
NS within the
rst hour and
55.4±17.5years Received
and had
abdominal
pain less
132 AP patients
Single-
center
RCT
3mL/kg/h
until oral
feeding
3mL/kg/h
until oral
feeding
than 24h
de Madaria
etal. (2018)
[87], Spain
Karki etal.
(2022) [88],
Nepal
Kayhan
etal. (2021)
[89], Turkey
RCT randomized controlled trials, AP acute pancreatitis, NS normal saline, LR lactated Ringer’s, CRP C-reactive protein
242
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L. Ke et al.
4.2 Renal Replacement Therapy
When AKI has already developed, the principles
of management are largely similar to AKI in
other disease settings, namely, supportive and
replacement treatment when necessary. For the
timing and indication of renal replacement therapy (RRT), since there is no high-quality evidence supporting the use of RRT for nonrenal
replacement purposes (including a promising
role in removing Inammatory mediators and
maintenance of acid-base status, for instance),
the application of RRT should be limited to
patients with severe AKI, evidenced by anuria
(negligible urine output for 6h), severe metabolic
acidosis (pH <7.2 with normal arterial PCO2),
severe volume overload (pulmonary edema), and
pronounced azotemia (blood urea nitrogen
>30mmol/L or creatinine >300 mol/L) [47]. In
recent years, with the emergence of new evidence, there has been a trend toward postponing
RRT in critically ill patients with AKI since the
delay strategy can signicantly reduce the
requirement of RRT without impacting clinical
outcomes [48] . However, since there are no studies addressing this question in AP patients, no
recommendations can be given regarding delaying RRT.
5 Management ofAcute
Cardiovascular Failure
During AP, acute cardiovascular (CVS) failure
or shock is often caused by noncardiac factors
and usually a combination of hypovolemia and
distributive shock (Fig. 2). On the one hand,
uid sequestration due to third spacing is typical
in AP, resulting in ascites and pleural effusion,
which are well-recognized early events during
AP [49]. Moreover, nausea and vomiting may
also contribute to volume depletion in AP.Several
parameters representing hemoconcentration,
like increased hematocrit, blood urea nitrogen,
or creatinine levels, have been found to predict a
more severe course of AP [50]. Further, local
pancreatic inammation results in the release of
cytokines, pro-inammatory mediators, and
other vasodilators like substance P and nitric
oxide [51], which can exacerbate inadequate
intravascular volume. Another factor is the
marked decrease in response to endogenous
vasopressors observed in AP [52], thought to be
due to endothelin and renin occupying receptors
for endogenous vasoconstrictors. In summary,
CVS failure in AP is caused by multiple pathophysiological processes and, therefore, needs to
be addressed with a multimodel approach to
management.
5.1 Fluid Resuscitation/Therapy
The treatment of acute CVS failure should start
with uid replacement since hypovolemia and
shock are common features of the pathogenesis
of AP.Current guidelines recommend a moderately aggressive and goal-directed uid approach,
initiating a rate of 5–10 mL/kg of body weight
[42]. The goals recommended for this approach
include heart rate, mean arterial pressure, urine
output, and hematocrit [42]. A major safety concern with uid resuscitation is overload and the
development of pleural effusion, pulmonary
edema, and ascites, in addition to edema within
end organs themselves. A recently published
large trial (the WATERFALL trial) in mainly
patients with mild AP conrmed that early
aggressive uid resuscitation (which was a bolus
of 20mL/kg in the rst 2 h followed by 3 mL/
kg/h), despite it being a previous standard of
care, resulted in a higher incidence of uid overload and did not improve outcomes [53]. There
are several previous studies that had previously
demonstrated that aggressive uid resuscitation
increased rates of organ failure and mortality in
patients with AP [54–56]. The conclusion from
these studies is that a moderate uid rate
(5–10mg/kg) should be used to address hypovolemia in the initial stage of resuscitation.
Determining ongoing uid requirements beyond
that, the so-called optimization phase of uid
resuscitation [57], requires more research, especially with the development of capillary leak syndrome [10] and the adverse clinical consequences
of excess interstitial uid.
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243
Fig. 2 Combined distributive shock and hypovolemic
shock in acute pancreatitis. The circulatory failure during
acute pancreatitis results from both mechanisms. Multiple
vasodilators like nitric oxide and substance P are released
into the circulation from the pancreas in acute pancreati-
5.2 The Use ofVasoactive Drugs
As CVS failure in AP has characteristics of both
hypovolemia and vasodilation, vasopressors are
commonly applied after initial uid resuscitation.
There are some controversies regarding the use
of vasoactive drugs in AP patients, especially in
regard to the optimal timing of administration. In
light of the consequences of aggressive uid
resuscitation [53], the early addition of vasopressors may help reduce the volume of uid resuscitation required and may result in better outcomes
[58]. However, vasopressors can compromise
gastrointestinal perfusion [59] in patients who
are already at risk of mucosal ischemia secondary to reex splanchnic vasoconstriction in hypo-
tis, leading to a fall in arterial pressure. In addition, due to
the increased vascular permeability, “third spacing” is a
common phenomenon in acute pancreatitis, which exacerbates circulatory failure
volemic AP patients. This gut injury contributes
to systemic inammation, bacterial translocation,
secondary infection, and end-organ dysfunction/
failure and is mediated through the lymphatic
system more than the portal venous system [13].
For the specic selection of available vasopressors, based on evidence across multiple
shock populations (including septic, hemorrhagic, and cardiogenic shock [59]), norepinephrine should be the rst-line choice mainly because
it improves coronary blood ow and microcirculation [60]. Overall, due to the lack of evidence
specically in AP patients, the use of vasopressors mostly depends on local practice and the
treating clinician (timing and type), and studies
are urgently needed in this eld.
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