Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / @xirurgi_2025 / @xirurgi_2025 - 971 - файл
.pdf
244
https://t.me/med1917
L. Ke et al.
6 Gastrointestinal Failure
andManagement
Gastrointestinal dysfunction is common in critically ill patients and is often subclinical and
underdiagnosed. Gastrointestinal function is not
as immediately necessary for life as other vital
organs, such as the heart and lungs, and perfusion
of these organs is prioritized. Splanchnic vasoconstriction, in response to hypovolemia in AP
patients, causes ischemic gut injury, resulting in
gastrointestinal dysfunction, the loss of barrier
function, and systemic exposure to toxic inammatory mediators from the microbiome, activated
pancreatic enzymes, and the injured gut wall.
There is a reciprocal and damaging relationship
between OF in other organ systems and gut
injury.
During AP, the gastrointestinal tract is inevitably and immediately affected by the local inammatory effusion of the pancreas. The released
pancreatic enzymes and inammatory mediators
can directly track through the mesentery and
involve the bowels. In a magnetic resonance
imaging (MRI) study conducted by Ji et al., it
was found that thickened bowel walls, mural
stratication, and dilation of the gastrointestinal
tract are common in AP patients and related to
clinical outcomes [61]. When the mesenteric vessels get involved by the inammatory process
initiated from the pancreas, blood supply to the
corresponding bowel segment is impaired, compounding ischemia and occasionally leading to
life-threatening bowel necrosis. In a single-center
prospective clinical study, Rahman etal. demonstrated that gastrointestinal failure, as reected
by the gastrointestinal failure score [62], was a
common organ failure in AP, and its severity was
associated with mortality [63].
6.1 Diagnosis, Monitoring,
andSeverity Assessment
Although not included in RAC as a named organ
failure, gastrointestinal failure is an important and
outcome-related organ failure worth more atten-
tion. The difculty might lie in the lack of assessment tools, and the recently established
Gastrointestinal Dysfunction Score (GIDS) may
help improve the objectivity for both research and
clinical use. The feasibility and accuracy of the
GIDS in the AP population should be tested in
future studies [64]. Gastric residual volume (GRV)
is a traditional marker reecting gastrointestinal
dysfunction, but the reliability of this marker was
questioned, and there is no agreement on the optimal cutoff to diagnose feeding intolerance [65]. In
a prospective study, Lin et al. used GRV
>500mL/6h as part of the diagnostic criteria for
feeding intolerance in nasogastric feeding moderately severe to severe AP patients, and the incidence was approximately 25% in this cohort [66].
Abdominal ultrasonography may be helpful as a
convenient tool for assessing gastrointestinal function and is widely available in ICUs. Gao etal.
proposed a quantitive score for bedside evaluation
called the acute gastrointestinal injury ultrasonography (AGIUS) score, incorporating the diameter,
thickness, and movement of the intestine [67].
Their results showed that the AGIUS score correlated well with the conventional gastrointestinal
failure score [62] and may serve as a useful tool
for point-of-care evaluation.
6.2 Drugs Associated
withGastrointestinal
Dysfunction
Antibiotics are widely used in managing AP for
either prophylactic or therapeutic purposes and
are essential for treating infected pancreatic
necrosis [68]. However, long-course antibiotics
are associated with potential adverse events,
including increased prevalence of multidrugresistant bacteria, higher risk of fungal infection,
and dysbiosis, which might be associated with
short-term and long-term detrimental effects
[69]. In this regard, prophylactic antibiotics are
not recommended in patients with AP because
they were not associated with improved clinical
outcomes [70] and because of the potential risks
mentioned above (Chap.12).
Managing Organ Failure inAcute Pancreatitis
https://t.me/med1917
245
On the other hand, analgesic therapy is a cornerstone in the early treatment of AP, and opioids
are commonly prescribed, especially for those
requiring mechanical ventilation. However, opioids can cause signicant and varying gastrointestinal symptoms, including nausea, vomiting,
immotility, and diarrhea [71], and a large cohort
study showed that increased opioid use was associated with prolonged hospital stay (Chap. 9).
Therefore, non-opioids should be considered for
analgesic therapy in AP. A recent meta-analysis
showed that nonsteroidal anti-inammatory
drugs (NSAIDs) and epidural administration of
local anesthetics might be effective adjuncts to
opioids in the pain management of AP patients
[72], though the evidence level is still low and
future large studies are warranted.
6.3 Drainage ofAscites
Ascites is a common occurrence in AP patients
during the rst week of disease onset, with an
incidence varying from 38.5% [73] to 60% [74],
depending on the severity of the patients. The
presence of ascites was associated with increased
mortality and longer duration of mechanical ventilation [73]. A retrospective cohort study of 102
patients showed that drainage of ascites was
associated with reduced inammatory markers,
delayed or less organ failure, and reduced need
for retroperitoneal intervention. Moreover,
another observational study addressed the most
signicant safety concern of early paracentesis
by showing that it did not increase the incidence
of infectious complications and infection-related
mortality [75]. However, since there is a lack of
randomized controlled trials concerning this
topic, early paracentesis is not recommended in
routine practice. For peritoneal lavage, which
used to be a common practice in the early treatment of AP, a meta-analysis found that early
lavage may not confer clinical benets and may
be associated with increased complications [76].
Therefore, lavage should not be routinely applied
to AP patients before new evidence emerges.
6.4 Early Enteral Nutrition
In the management of AP, early enteral nutrition
(EN) is considered essential because it helps
maintain the function and structure of the gastrointestinal mucosa, preserving the integrity of
intestinal barrier function and preventing bacterial translocation [77] (see Chap. 11). This
“EN-rst” approach goes against the conventional “pancreatic rest” and “bowel rest” theories,
which state that EN increases the secretion of
pancreatic enzymes to increase the severity of AP
[78]. However, it is shown that pancreatic exocrine function is diminished proportionally to the
morphologic destruction of the pancreas during
AP episodes, especially severe in patients with
pancreatic necrosis [79]. Based on this evidence,
EN should not stimulate pancreatic secretion,
especially in acute necrotizing pancreatitis. More
importantly, numerous studies have shown that
compared with early parenteral nutrition or
delayed EN, early EN is associated with lower
mortality, organ failure, infection of pancreatic
necrosis and extrapancreatic sites, and the
requirement for invasive interventions (Table2).
In practice, due to the frequent presence of IAH
and impaired gastrointestinal motility, the implementation of EN in AP can be challenging, and
caution is advised. The 2020 ESPEN guidelines
divided AP patients into predicted “mild to moderate” and “severe” and recommended different
approaches. Severe AP is considered at nutrition
risk regardless of pre-admission nutrition status
due to enhanced catabolism. In patients who
cannot be orally fed, the guidelines recommend
that EN should be started early, within 24–72h
of admission. During the acute phase of AP, EN
intake should gradually increase over the rst 3 to
4days to reach the feeding target [80]. Because
EN can cause an increase in IAP, caution is
needed when IAP reaches 15mmHg and over. In
this population, the majority of the patients have
different degrees of gastrointestinal failure characterized by the absence of bowel movement,
abdominal distention, and high gastric residual
volumes, and the guidelines recommend that the
246
https://t.me/med1917
Primary
outcome Main ndings
Not stated • Patients who received enteral feeding experienced
fewer total complications (P<0.05) and were at a
lower risk of developing septic complications
(P<0.01) than those receiving parenteral nutrition
• The cost of nutritional support was three times higher
faster than PN patients (p=0.09)
in patients who received parenteral nutrition
• C-reactive protein in EN patients was reduced by 50%
• Both groups received a similar number of kilojoules
Days to
achieve a 50%
reduction in
and achieved near normal prealbumin and 24-h urinary
nitrogen values
group)
• Overall mortality was 4.9% (3 patients in the PN
C-reactive
protein levels
was signicantly lower in the enterally fed group (7 vs.
• Nine EN patients dislodged the nasojejunal tube
16, p=0.02)
• The incidence of pancreatic infectious complications
Incidence of
pancreatic
infectious
group and 12in the TPN group (p<0.01)
• Overall mortality was 20% with 2 deaths in the TEN
complications
groups in the APACHE II score; in CRP, TNF-α, and
Not stated • No signicant differences were found between the two
IL-6 concentrations; or in prealbumin and albumin
levels over the rst 10days
hospitalization
• Length of hospital stay was alike in the two groups
• Two patients from group 1 died in the course of the
L. Ke et al.
protein values in both the enteral nutrition group and
the total parenteral nutrition group at 1week and
2weeks (P<0.001 for both)
intervention (56.0 vs. 60.0%; P=1.000), infective
complications (64.0 vs. 60.0%; P=1.000), or mortality
(20.0 vs. 16.0%; P=1.000) in enteral nutrition vs. total
• There was no signicant difference in surgical
Not stated • There was a signicant decrease in serum C-reactive
parenteral nutrition, respectively
PN (20
pts)
pts)
65.2±9.9 EN (18
necrotizing
pancreatitis
38 Severe
Single- center
RCT
PN (18
pts)
pts)
61.25±16.4 EN (10
Ranson score
of 3 or greater
28 AP with a
Multicenter
RCT
TPN (34
pts)
TEN (35
pts)
Median (range):
51 (42–67) for
TEN patients, 52
(41–70) for TPN
patients
within 72h of
the onset of
symptoms
70 Predicted SAP
Single- center
RCT
TEN (11
pts)
pts)
58.4±16 TPN (11
criteria)
RCT 22 SAP (Atlanta
PN (25
pts)
pts)
39.75±12.6 EN (25
criteria) with a
CTSI equal to
or greater than
50 SAP (Atlanta
A single-
center,
prospective
clinical trial
7
First author
(year), country Study design n Population Age Group 1 Group 2
Kalfarentzos
Table 2 Randomized trials comparing enteral nutrition vs. parenteral nutrition in acute pancreatitis
etal. (1997)
[90], Greece
Louie etal.
(2005) [91],
Vancouver, BC
Petrov etal.
(2006) [92],
Russia
Casas etal.
(2007) [93],
Spain
Doley etal.
(2009) [94],
India
Managing Organ Failure inAcute Pancreatitis
https://t.me/med1917
failure and 3 developed non-respiratory single organ
failure. There were no such complications in the TEN
nutrition-related complications
• In the TPN group, 3 patients developed respiratory
group
• The cost of TEN was considerably less than that of
according to the revised Atlanta classication (22
patients), and gastrointestinal symptoms or abdominal
TPN
pain did not signicantly differ between the groups
• PEG, EndoCAb, CRP, IL-6, APACHE II score, severity
• Total complications (25 vs. 52; P=0.04) and
pulmonary complications (10 vs. 21; P=0.04) were
improved in the enterally fed patients
signicantly more frequent in EN patients, although
complications were diagnosed dominantly within the
rst 3days
necrosis, abscess) was lower in the enteral group
(P=0.08)
EndoCAb antibodies and an increase in TAC
• SIRS, sepsis, organ failure, and ICU stay were globally
• Enterally fed patients showed no change in the level of
in the group with total parenteral nutrition, which was
higher than that in the group with total enteral nutrition
(21%)
247
group with total enteral nutrition (23%) was lower than
that in the group with total parenteral nutrition (72%, P
• The incidence of pancreatic septic necroses in the
G 0.05)
Not stated • All patients tolerated the feeding regime well with few
TPN (9
pts)
TEN (8
pts)
Median (range):
65 (56–89) for EN
patients, 57
(38–86) for PN
patients
with the
presence of an
APACHE II of
6 or more
21 Predicted SAP
Single- center
RCT
Intestinal
permeability
measured by
excretion of
polyethylene
TPN (26
pts)
EN (24
pts)
71 (58–80) for EN
patients,
68 (60–80) for PN
patients
50 Predicted SAP Median (IQR):
A single-
center,
prospective
randomized
study
glycol (PEG)
in urine
Not stated • The rate of septic complications (infected pancreatic
PN (48
pts)
EN (41
pts)
47.2 (mean) for
EN patients, 43.8
(mean) for PN
within 24 to
72h after the
89 AP admitted
Single- center
RCT
Incidence of
the systemic
PN (18
pts)
EN (16
pts)
patients
Median (IQR): 63
(47–76) for EN
onset of
symptoms
after admission
RCT 34 AP within 48h
inammatory
response
syndrome
None • Eighty percent of the patients developed organ failure
TPN (54
patients, 63
(52–73) for PN
patients
53±11.6 TEN (53
107 ANP within
Single- center
pts)
pts)
48h after the
onset of the
disease
RCT
Gupta etal.
(2003) [95], UK
Eckerwall etal.
(2006) [96],
Sweden
Olah etal.
(2002) [97],
Hungary
Windsor etal.
(1998) [98], UK
Wu etal. (2010)
[99], China
RCT randomized controlled trials, AP acute pancreatitis, SAP severe acute pancreatitis, EN enteral nutrition, PN parenteral nutrition. TEN total enteral nutrition, TPN total par-
enteral nutrition
248
https://t.me/med1917
L. Ke et al.
nasojejunal route is preferred over the nasogastric route despite the RCTs showing no difference between nasojejunal and nasogastric routes
in severe AP patients [81]. Taken together, when
implementing early EN in AP patients, always
keep IAP and gastrointestinal dysfunction in
mind and monitor them frequently.
6.5 Assessment andTreatment
ofEnteral Feeding Intolerance
Feeding intolerance is common when implementing EN [66] or taking oral diet [82] in AP
patients and is associated with more severe
disease and unfavorable outcomes. There is no
universal tool to assess feeding intolerance in AP;
thus the denitions of intolerance varyes between
different studies. Generally, patients who report
worsening symptoms (including abdominal distension, pain, vomiting) had increased IAP, and/
or cannot reach the nutrition target, and an alternative approach to nutritional support should be
considered.
The use of prokinetics appears to make sense
in patients with feeding intolerance. In critically
ill patients, a meta-analysis showed that prokinetic agents could reduce feeding intolerance, but
its impact on clinical outcomes like mortality and
length of ICU stay remains unclear [83].
However, the evidence for prokinetics in AP
patients is sparse, and further studies are needed.
7 Hepatic andOther Organ
Failures
For other organ systems, liver failure and central
nervous system failure are relatively uncommon
in AP and are usually due to extrapancreatic
causes. The management of these organ failures
should follow the relevant guidelines for critically ill patients.
8 Conclusion
In conclusion, the development, number and duration of organ failure are the most important determinants of severity and outcome in AP.Although
the clinical characteristics are similar to organ failure in other critical illnesses, AP-associated organ
failure has a unique combination of challenges,
including systemic inammation, intra- abdominal
pressure, compromised mesenteric perfusion associated with gastrointestinal failure, hypovolemia,
and distributive shock. The management of
AP-associated organ failure requires expertise to
optimize organ function and avoid iatrogenic
injury, especially as there is an urgent need for better quality evidence in a number of areas highlighted in this chapter.
References
1. Banks PA, Bollen TL, Dervenis C, etal. Classication
of acute pancreatitis—2012: revision of the Atlanta
classication and denitions by international consensus. Gut. 2013;62:102–11.
2. Dellinger EP, Forsmark CE, Layer P, et al.
Determinant-based classication of acute pancreatitis
severity: an international multidisciplinary consultation. Ann Surg. 2012;256:875–80.
3. Petrov MS, Shanbhag S, Chakraborty M, etal. Organ
failure and infection of pancreatic necrosis as determinants of mortality in patients with acute pancreatitis. Gastroenterology. 2010;139:813–20.
4. van Santvoort HC, Besselink MG, Bakker OJ, etal. A
step-up approach or open necrosectomy for necrotizing pancreatitis. N Engl J Med. 2010;362:1491–502.
5. van Brunschot S, van Grinsven J, van Santvoort HC,
et al. Endoscopic or surgical step-up approach for
infected necrotising pancreatitis: a multicentre randomised trial. Lancet. 2018;391:51–8.
6. Sternby H, Bolado F, Canaval-Zuleta HJ, et al.
Determinants of severity in acute pancreatitis: a
nation-wide multicenter prospective cohort study.
Ann Surg. 2019;270:348–55.
7. Shi N, Liu T, de la Iglesia-Garcia D, etal. Duration of
organ failure impacts mortality in acute pancreatitis.
Gut. 2020;69:604–5.
8. Machicado JD, Gougol A, Tan X, etal. Mortality in
acute pancreatitis with persistent organ failure is determined by the number, type, and sequence of organ
systems affected. United European Gastroenterol J.
2021;9:139–49.
9. Raraty MG, Connor S, Criddle DN, et al. Acute
pancreatitis and organ failure: pathophysiology,
natural history, and management strategies. Curr
Gastroenterol Rep. 2004;6:99–103.
10. Komara NL, Paragomi P, Greer PJ, etal. Severe acute
pancreatitis: capillary permeability model linking systemic inammation to multiorgan failure. Am J Physiol
Gastrointest Liver Physiol. 2020;319:G573–83.
11. Kinnala PJ, Kuttila KT, Gronroos JM, etal. Splanchnic
and pancreatic tissue perfusion in experimental acute
pancreatitis. Scand J Gastroenterol. 2002;37:845–9.
Managing Organ Failure inAcute Pancreatitis
https://t.me/med1917
249
12. Cuthbertson CM, Christophi C. Disturbances of the
microcirculation in acute pancreatitis. Br J Surg.
2006;93:518–30.
13. Windsor JA, Trevaskis NL, Phillips AJ. The gutlymph model gives new treatment strategies for organ
failure. JAMA Surg. 2022;157:540–1.
14. Schepers NJ, Bakker OJ, Besselink MG, etal. Impact
of characteristics of organ failure and infected necrosis on mortality in necrotising pancreatitis. Gut.
2019;68:1044–51.
15. Qu C, Zhang H, Chen T, etal. Early on-demand drainage versus standard management among acute necrotizing pancreatitis patients complicated by persistent
organ failure: the protocol for an open-label multicenter randomized controlled trial. Pancreatology.
2020;20:1268–74.
16. Bang JY, Arnoletti JP, Holt BA, et al. An endoscopic transluminal approach, compared to minimally invasive surgery, reduces complications and
costs for patients with necrotizing pancreatitis.
Gastroenterology. 2019;156(4):1027–40.
17. Lambden S, Laterre PF, Levy MM, et al. The SOFA
score-development, utility and challenges of accurate
assessment in clinical trials. Crit Care. 2019;23:374.
18. Mounzer R, Langmead CJ, Wu BU, etal. Comparison
of existing clinical scoring systems to predict persistent organ failure in patients with acute pancreatitis.
Gastroenterology. 2012;142:1476–82; quiz e15–6
19. Seymour CW, Liu VX, Iwashyna TJ, etal. Assessment
of clinical criteria for sepsis: for the third international
consensus denitions for sepsis and septic shock
(Sepsis-3). JAMA. 2016;315:762–74.
20. Rasch S, Pichlmeier EM, Phillip V, etal. Prediction of
outcome in acute pancreatitis by the qSOFA and the
new ERAP score. Dig Dis Sci. 2022;67:1371–8.
21. Shi N, Zhang X, Zhu Y, etal. Predicting persistent
organ failure on admission in patients with acute
pancreatitis: development and validation of a mobile
nomogram. HPB (Oxford). 2022;24:1907–20.
22. Gajendran M, Prakash B, Perisetti A, etal. Predictors
and outcomes of acute respiratory failure in hospitalised patients with acute pancreatitis. Frontline
Gastroenterol. 2021;12:478–86.
23. Li L, Liu S, Zhang X, et al. Predicting persistent
acute respiratory failure in acute pancreatitis: the
accuracy of two lung injury indices. Dig Dis Sci.
2023;68:2878–89.
24. Working Party of the British Society of G, Association
of Surgeons of Great B, Ireland, et al. UK guidelines for the management of acute pancreatitis. Gut.
2005;54 Suppl 3:iii1–9.
25. Paraskevas T, Oikonomou E, Lagadinou M, etal. The
role of high ow nasal oxygen in the management of
severe COVID-19: a systematic review. Acta Medica
Port. 2022;35:476–83.
26. Ji X, Zhou J, Wu W, etal. Application of high-ow
oxygen therapy in acute pancreatitis complicated
with acute respiratory dysfunction. Turk J Med Sci.
2022;52:707–14.
27. Chen C, Xia SH, Chen H, et al. Therapy for acute
pancreatitis with platelet-activating factor receptor
antagonists. World J Gastroenterol. 2008;14:4735–8.
28. Johnson CD, Kingsnorth AN, Imrie CW, etal. Double
blind, randomised, placebo controlled study of a
platelet activating factor antagonist, lexipafant, in the
treatment and prevention of organ failure in predicted
severe acute pancreatitis. Gut. 2001;48:62–9.
29. Abu-Zidan FM, Windsor JA. Lexipafant and acute
pancreatitis: a critical appraisal of the clinical trials.
Eur J Surg. 2002;168:215–9.
30. Szatmary P, Grammatikopoulos T, Cai W, et al.
Acute pancreatitis: diagnosis and treatment. Drugs.
2022;82:1251–76.
31. Ke L, Ni HB, Sun JK, etal. Risk factors and outcome of
intra-abdominal hypertension in patients with severe
acute pancreatitis. World J Surg. 2012;36:171–8.
32. Pelosi P, Quintel M, Malbrain ML. Effect of intraabdominal pressure on respiratory mechanics. Acta
Clin Belg Suppl. 2007;62:78–88.
33. Ke L, Tong ZH, Ni HB, et al. The effect of intraabdominal hypertension incorporating severe
acute pancreatitis in a porcine model. PLoS One.
2012;7:e33125.
34. Fan E, Del Sorbo L, Goligher EC, etal. An Ofcial
American Thoracic Society/European Society of
Intensive Care Medicine/Society of Critical Care
Medicine Clinical Practice Guideline: Mechanical
Ventilation in Adult Patients with Acute Respiratory
Distress Syndrome. Am J Respir Crit Care Med.
2017;195:1253–63.
35. Acute Respiratory Distress Syndrome N, Brower RG,
Matthay MA, etal. Ventilation with lower tidal volumes as compared with traditional tidal volumes for
acute lung injury and the acute respiratory distress
syndrome. N Engl J Med. 2000;342:1301–8.
36. *Talmor D, Sarge T, Malhotra A, etal. Mechanical
ventilation guided by esophageal pressure in acute
lung injury. N Engl J Med 2008;359:2095–2104.
*This study showed that a ventilator strategy using
esophageal pressures to estimate the trans-pulmonary
pressure signicantly improves oxygenation and
compliance.
37. Regli A, Pelosi P, Malbrain M.Ventilation in patients
with intra-abdominal hypertension: what every critical care physician needs to know. Ann Intensive Care.
2019;9:52.
38. Kirkpatrick AW, Roberts DJ, De Waele J, etal. Intraabdominal hypertension and the abdominal compartment syndrome: updated consensus denitions and
clinical practice guidelines from the World Society
of the Abdominal Compartment Syndrome. Intensive
Care Med. 2013;39:1190–206.
39. Jena A, Singh AK, Kochhar R. Intra-abdominal
hypertension and abdominal compartment syndrome in acute pancreatitis. Indian J Gastroenterol.
2023;42:455–66.
40. Schmandt M, Glowka TR, Kreyer S, etal. Secondary
ARDS following acute pancreatitis: is extracorporeal
250
https://t.me/med1917
L. Ke et al.
membrane oxygenation feasible or futile? J Clin Med.
2021;10:1000.
41. Machicado JD, Papachristou GI. Intravenous uid
resuscitation in the management of acute pancreatitis.
Curr Opin Gastroenterol. 2020;36:409.
42. Working Group IAPAPAAPG. IAP/APA evidencebased guidelines for the management of acute pancreatitis. Pancreatology. 2013;13:e1–15.
43. Vedantam S, Tehami N, de Madaria E, etal. Lactated
ringers does not reduce SIRS in acute pancreatitis
compared to normal saline: an updated meta-analysis.
Dig Dis Sci. 2022;67(7):3265–74.
44. Ye B, Huang M, Chen T, et al. The impact of normal saline or balanced crystalloid on plasma chloride
concentration and acute kidney injury in patients
with predicted severe acute pancreatitis: protocol
of a phase II, multicenter, stepped-wedge, clusterrandomized, controlled trial. Front Med (Lausanne).
2021;8:731955.
45. Ye B, Mao W, Chen Y, et al. Aggressive resuscitation is associated with the development of acute
kidney injury in acute pancreatitis. Dig Dis Sci.
2019;64:544–52.
46. Gad MM, Simons-Linares CR. Is aggressive intravenous uid resuscitation benecial in acute pancreatitis? A meta-analysis of randomized control
trials and cohort studies. World J Gastroenterol.
2020;26:1098–106.
47. Bellomo R, Kellum JA, Ronco C.Acute kidney injury.
Lancet. 2012;380:756–66.
48. Li X, Liu C, Mao Z, et al. Timing of renal replacement therapy initiation for acute kidney injury in critically ill patients: a systematic review of randomized
clinical trials with meta-analysis and trial sequential
analysis. Crit Care. 2021;25:15.
49. Maringhini A, Ciambra M, Patti R, et al. Ascites,
pleural, and pericardial effusions in acute pancreatitis.
A prospective study of incidence, natural history, and
prognostic role. Dig Dis Sci. 1996;41:848–52.
50. Haydock MD, Mittal A, Wilms HR, etal. Fluid therapy in acute pancreatitis: anybody’s guess. Ann Surg.
2013;257:182–8.
51. Garcia M, Calvo JJ. Cardiocirculatory pathophysiological mechanisms in severe acute pancreatitis.
World J Gastrointest Pharmacol Ther. 2010;1:9–14.
52. Garcia M, Hernandez-Barbachano E, Hernandez
Lorenzo MP, et al. Cardiovascular homeostasis in
hypotension associated with initial stages of severe
acute pancreatitis. Pancreas. 2008;37:432–9.
53. de Madaria E, Buxbaum JL, Maisonneuve P, et al.
Aggressive or moderate uid resuscitation in acute
pancreatitis. N Engl J Med. 2022;387:989–1000.
54. Jin T, Jiang K, Deng L, et al. Response and outcome from uid resuscitation in acute pancreatitis: a prospective cohort study. HPB (Oxford).
2018;20:1082–91.
55. Mao EQ, Fei J, Peng YB, etal. Rapid hemodilution is
associated with increased sepsis and mortality among
patients with severe acute pancreatitis. Chin Med J.
2010;123:1639–44.
56. de Madaria E, Soler-Sala G, Sanchez-Paya J,
et al. Inuence of uid therapy on the prognosis of
acute pancreatitis: a prospective cohort study. Am J
Gastroenterol. 2011;106:1843–50.
57. Hoste EA, Maitland K, Brudney CS, etal. Four phases
of intravenous uid therapy: a conceptual model. Br J
Anaesth. 2014;113:740–7.
58. Russell JA.Vasopressor therapy in critically ill patients
with shock. Intensive Care Med. 2019;45:1503–17.
59. Jozwiak M, Geri G, Laghlam D, et al. Vasopressors
and risk of acute mesenteric ischemia: a worldwide
pharmacovigilance analysis and comprehensive literature review. Front Med (Lausanne). 2022;9:826446.
60. Georger JF, Hamzaoui O, Chaari A, et al. Restoring
arterial pressure with norepinephrine improves
muscle tissue oxygenation assessed by near-infrared
spectroscopy in severely hypotensive septic patients.
Intensive Care Med. 2010;36:1882–9.
61. Ji YF, Zhang XM, Mitchell DG, etal. Gastrointestinal
tract involvement in acute pancreatitis: initial ndings
and follow-up by magnetic resonance imaging. Quant
Imaging Med Surg. 2017;7:641–53.
62. Reintam A, Parm P, Kitus R, et al. Gastrointestinal
failure score in critically ill patients: a prospective
observational study. Crit Care. 2008;12:R90.
63. Rahman A, Hasan RM, Agarwala R, etal. Identifying
critically-ill patients who will benet most from nutritional therapy: further validation of the “modied
NUTRIC” nutritional risk assessment tool. Clin Nutr.
2016;35:158–62.
64. Reintam Blaser A, Padar M, Mandul M, et al.
Development of the gastrointestinal dysfunction score
(GIDS) for critically ill patients—a prospective multicenter observational study (iSOFA study). Clin Nutr.
2021;40:4932–40.
65. Elke G, Felbinger TW, Heyland DK.Gastric residual
volume in critically ill patients: a dead marker or still
alive? Nutr Clin Pract. 2015;30:59–71.
66. Lin J, Lv C, Wu C, etal. Incidence and risk factors of
nasogastric feeding intolerance in moderately-severe
to severe acute pancreatitis. BMC Gastroenterol.
2022;22:327.
67. Gao T, Cheng MH, Xi FC, etal. Predictive value of
transabdominal intestinal sonography in critically ill
patients: a prospective observational study. Crit Care.
2019;23:378.
68. Severino A, Varca S, Airola C, et al. Antibiotic utilization in acute pancreatitis: a narrative review.
Antibiotics (Basel). 2023;12:1120.
69. Patangia DV, Anthony Ryan C, Dempsey E, et al.
Impact of antibiotics on the human microbiome
and consequences for host health. Microbiol Open.
2022;11:e1260.
70. Leppaniemi A, Tolonen M, Tarasconi A, et al. 2019
WSES guidelines for the management of severe acute
pancreatitis. World J Emerg Surg. 2019;14:27.
71. Camilleri M, Lembo A, Katzka DA.Opioids in gastroenterology: treating adverse effects and creating
therapeutic benets. Clin Gastroenterol Hepatol.
2017;15:1338–49.
Managing Organ Failure inAcute Pancreatitis
https://t.me/med1917
251
72. Thavanesan N, White S, Lee S, etal. Analgesia in the
initial management of acute pancreatitis: a systematic
review and meta-analysis of randomised controlled
trials. World J Surg. 2022;24:S241.
73. Samanta J, Rana A, Dhaka N, etal. Ascites in acute
pancreatitis: not a silent bystander. Pancreatology.
2019;19:646–52.
74. Dugernier T, Laterre PF, Reynaert MS.Ascites uid
in severe acute pancreatitis: from pathophysiology to
therapy. Acta Gastroenterol Belg. 2000;63:264–8.
75. Liu L, Yan H, Liu W, et al. Abdominal paracentesis
drainage does not increase infection in severe acute
pancreatitis: a prospective study. J Clin Gastroenterol.
2015;49:757–63.
76. Dong Z, Petrov MS, Xu J, etal. Peritoneal lavage for
severe acute pancreatitis: a systematic review of randomised trials. World J Surg. 2010;34:2103–8.
77. Jablonska B, Mrowiec S. Nutritional support in
patients with severe acute pancreatitis-current standards. Nutrients. 2021;13:1498.
78. Petrov MS.Gastric feeding and “gut rousing” in acute
pancreatitis. Nutr Clin Pract. 2014;29:287–90.
79. O’Keefe SJ, Lee RB, Li J, et al. Trypsin secretion
and turnover in patients with acute pancreatitis. Am J
Physiol Gastrointest Liver Physiol. 2005;289:G181–7.
80. Arvanitakis M, Ockenga J, Bezmarevic M, et al.
ESPEN guideline on clinical nutrition in acute and
chronic pancreatitis. Clin Nutr. 2020;39:612–31.
81. Nally DM, Kelly EG, Clarke M, et al. Nasogastric
nutrition is efcacious in severe acute pancreatitis:
a systematic review and meta-analysis. Br J Nutr.
2014;112:1769–78.
82. Pothoulakis I, Nawaz H, Paragomi P, etal. Incidence
and risk factors of oral feeding intolerance in acute
pancreatitis: results from an international, multicenter, prospective cohort study. United European
Gastroenterol J. 2021;9:54–62.
83. Lewis K, Alqahtani Z, McIntyre L, etal. The efcacy
and safety of prokinetic agents in critically ill patients
receiving enteral nutrition: a systematic review
and meta-analysis of randomized trials. Crit Care.
2016;20:259.
84. Wu BU, Hwang JQ, Gardner TH, et al. Lactated
Ringer’s solution reduces systemic inammation
compared with saline in patients with acute pancreatitis. Clin Gastroenterol Hepatol. 2011;9:710–717 e1.
85. Choosakul S, Harinwan K, Chirapongsathorn S, etal.
Comparison of normal saline versus lactated Ringer’s
solution for uid resuscitation in patients with mild
acute pancreatitis, a randomized controlled trial.
Pancreatology. 2018;18:507.
86. Lee A, Ko C, Buitrago C, et al. Lactated ringers
vs normal saline resuscitation for mild acute pancreatitis: a randomized trial. Gastroenterology.
2021;160:955–957 e4.
87. de Madaria E, Herrera-Marante I, Gonzalez-Camacho
V, et al. Fluid resuscitation with lactated Ringer’s
solution vs normal saline in acute pancreatitis: a
triple-blind, randomized, controlled trial. United
European. Gastroenterol J. 2018;6:63–72.
88. Karki B, Thapa S, Khadka D, etal. Intravenous ringers lactate versus normal saline for predominantly
mild acute pancreatitis in a Nepalese tertiary hospital.
PLoS One. 2022;17:e0263221.
89. Kayhan S, Selcan Akyol B, Ergul M, et al. The
effect of type of uid on disease severity in acute
pancreatitis treatment. Eur Rev Med Pharmacol Sci.
2021;25:7460–7.
90. Kalfarentzos F, Kehagias J, Mead N, et al. Enteral
nutrition is superior to parenteral nutrition in severe
acute pancreatitis: results of a randomized prospective
trial. Br J Surg. 1997;84:1665–9.
91. Louie BE, Noseworthy T, Hailey D, et al. 2004
MacLean-Mueller prize enteral or parenteral nutrition for severe pancreatitis: a randomized controlled
trial and health technology assessment. Can J Surg.
2005;48:298–306.
92. Petrov MS, Kukosh MV, Emelyanov NV. A randomized controlled trial of enteral versus parenteral
feeding in patients with predicted severe acute pancreatitis shows a signicant reduction in mortality
and in infected pancreatic complications with total
enteral nutrition. Dig Surg. 2006;23:336–44; discussion 344–5
93. Casas M, Mora J, Fort E, et al. Total enteral nutrition vs. total parenteral nutrition in patients with
severe acute pancreatitis. Rev Esp Enferm Dig.
2007;99:264–9.
94. Doley RP, Yadav TD, Wig JD, etal. Enteral nutrition
in severe acute pancreatitis. JOP. 2009;10:157–62.
95. Gupta R, Patel K, Calder PC, et al. A randomised
clinical trial to assess the effect of total enteral and
total parenteral nutritional support on metabolic,
inammatory and oxidative markers in patients with
predicted severe acute pancreatitis (APACHE II > or
=6). Pancreatology. 2003;3:406–13.
96. Eckerwall GE, Axelsson JB, Andersson RG. Early
nasogastric feeding in predicted severe acute pancreatitis: a clinical, randomized study. Ann Surg.
2006;244:959–65; discussion 965–7
97. Olah A, Pardavi G, Belagyi T, etal. Early nasojejunal
feeding in acute pancreatitis is associated with a lower
complication rate. Nutrition. 2002;18:259–62.
98. Windsor AC, Kanwar S, Li AG, etal. Compared with
parenteral nutrition, enteral feeding attenuates the
acute phase response and improves disease severity in
acute pancreatitis. Gut. 1998;42:431–5.
99. Wu XM, Ji KQ, Wang HY, et al. Total enteral nutrition in prevention of pancreatic necrotic infection in
severe acute pancreatitis. Pancreas. 2010;39:248–51.
Соседние файлы в папке @xirurgi_2025