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MANAGEMENT OF THE CRITICALLY ILL PATIENT WITH

SEVERE ACUTE PANCREATITIS

Iulian Stratan

WHAT IS ACUTE PANCREATITIS? SAP – MORTALITY RATE?


Acute pancreatitis is an acute inflammatory pro- The patients who require admission to an inten-
cess of the pancreas with variable involvement of sive care unit have mortality rates in the range of 30
other regional tissues or remote organ systems. – 50% and a mean hospital length of stay > 1 month.
In about 15-20% of patients with acute pancre- Mortality varies with etiology, the development of com-
atitis, severe damage to the pancreas may lead to a plication or necrosis and the number and severity of
life threatening illness that is often associated with co-morbid medical conditions.
prolonged hospitalization, multiple surgical procedure The cost of care for these patients is substantial,
and death in some patients. with estimates of total direct and indirect costs rang-
Severe acute pancreatitis (SAP) is a serious and ing from $ 3.6 billion to $ 6 billion annually.
life threatening disease and require intensive and ag-
gressive management of multiple organ failure and
Recommendation 1
severe infective complication that develop in these
The etiology of acute pancreatitis should be de-
patient. Many of the complications seen in severe
termined in at least 80% of cases and no more than
acute pancreatitis are associated with the presence
20% should be classified as idiopatic. (Grad B)
of the dead pancreatic tissue in the abdomen.
Patients with SAP may benefit from an environ-
This dead pancreas tissue is called pancreatic necro-
sis and the dead fatty around the pancreas is ment with more intensive monitoring given their po-
called peripancreatic necrosis. Severe acute pancre- tential for progressive organ dysfunction and/or life-
atitis usually develops when parts of the pan- threatening local complication but, avoiding unneces-
creas become necrotic (dead) from the acute inflam- sary ICU admission may limit the risk of nosocomial
mation. infection and iatrogenic complications.
Patients with SAP who fulfill conventional crite-
ria for ICU admission should be admitted as well as
WHAT IS PANCREATIC NECROSIS?
those patients at high risk of rapid deterioration (eld-
Severe pancreatitis causes death of parts of the erly, significant obesity, requiring ongoing volume re-
pancreas. The injured dying pancreas releases diges- suscitation and patient with evidence of substantial
tive enzymes in the gland, which causes extensive pancreatic necrosis).
death of fatty tissue in the abdomen. As a conse-
quence, patients with severe pancreatitis have dead Recommendation 2
pancreatic tissue and also widespread death of fatty Admission in ICU is recommended for patients
tissue around the pancreas. with SAP who fulfill conventional criteria for
ICU admission as well as those patients at high
risk of rapid deterioration (elderly ,significant obesity,
requiring ongoing volume resuscitation and patient
with evidence of substantial pancreatic necrosis
Anesthesiology and Intensive Care Department >30%).
University Hospital Saint Spiridon Iasi (Grad D, level 5 evidence)

166 Timi[oara, 2005


Recommendation 3 Should patients with severe acute pancreatitis
Critically ill patients with pancreatitis will be cared receive prophylactic antibiotics?
for by an intensivist leader, multidisciplinary team with Infection of necrotic pancreas develops in 30-
ready access to physicians skilled in endoscopy, ERCP, 50% of patients with necrosis documented by CT or
surgery, and interventional radiology. (Grad B, level surgery.
3a evidence) Infection might occur within first week, but its
incidence tend to peak in the third week of disease.
Recommendation 4 Rates of organ failure and mortality appear to
Close clinical observation of patients with pan- be highest among patients with infected pancreatic
creatitis is strongly recommended. These patients necrosis.
require early and aggressive fluid resuscitation. They The lack of any consistent benefit across stud-
are at the risk for the early development of organ ies, their variable inclusion criteria, variable method-
dysfunction as a result of inadequate resuscitation and ological quality, different antimicrobial regimen and
systemic and local complication of pancreatitis. the significant potential for harm preclude recommen-
Clinical monitoring should focus on intravascular dation for routine intravenous prophylactic antimicro-
volume assessment (physical examination, urine out- bial therapy in patients with SAP.
put, acid – base status) and pulmonary function. Prophylactic antimicrobial have been associated
(Grad D, level 5 evidence) with a change in the spectrum of pancreatic isolates
from enteric Gram - negative to fungi and Gram –
Recommendation 5 positive organisms.
Jury recommends against the routine use of
markers such CRP or procalcitonin to guide clinical Selective decontamination of digestive tract
decision making, predict the clinical course of pan- No further evidence has been published to sup-
creatitis or triage patients. (Grad D , level 5 evidence) port the one large randomized controlled trial which
has been conducted in patient with severe acute pan-
Recommendation 6 creatitis, to examine the effect of selective gut de-
In presence of diagnostic uncertain at the time contamination in combination with intravenous antibi-
of initial presentation, a CT scan of the abdomen (with otic on outcome in acute pancreatitis. In that study
intravenous contrast in the absence of contraindica- there was no statistically significant reduction in mor-
tion) may be performed after adequate fluid resusci- tality rate. It is no clear whether the reported benefit
tation to confirm the diagnostic of pancreatitis and to arose from the use of intravenous antibiotics or from
rule out alternate diagnosis. An admission CT scan gut decontamination.
may also serve as baseline for future scan. (Grad D,
level 5 evidence) Recommendation 8
No routine use of prophylactic systemic antibac-
Recommendation 7 terial or antifungal agents in patients with necrotizing
CT to identify local complications will be delayed pancreatitis in light of inconclusive and divided expert
for 48 -72 hrs when possible, as necrosis might not be opinion. Subsets of patients who benefit from pro-
visualized earlier. (Grad D, level 5 evidence) phylactic antibiotic may be identified by further in-
vestigation. (Grad B, level 2b evidence)

Summary of randomized trials examining routine prophylactic antibiotics for SAP:

Actualit\]i <n anestezie, terapie intensiv\ [i medicin\ de urgen]\ 167


What is the optimal mode and timing of nutri- lection and pancreatic necrosis is not necessary and
tional support for patients with SAP? may infect otherwise sterile tissues.
Patients with SAP are hypercatabolic; timely in- The presence of tissue necrosis further exacer-
stitution of feeding is important if malnutrition is to be bate or impairs the resolution of local and systemic
avoided or treated. A large body of evidence, sug- inflammatory response. Nonviable tissue might be
gests that there are several potential benefit from seeded be enteric organisms, resulted infected ne-
enteral nutrition compared with parenteral nutrition crosis. Necrosis in context of severe clinical disease
including a reduction in microbial translocation, im- mandates repeated assessment of need for interven-
proved in gut blood flow and preservation of gut mu- tion. Later in the disease, the necrotic pancreas de-
cosal surface immunity. marcates from viable tissue leading to an easier and
Eight trial have directly compared enteral nutri- safer debridement. Over time the aria of necrosis
tion and parenteral nutrition. undergoes liquefaction resulting an abscess that might
Two studies demonstrated an attenuated inflam- be more amenable to percutaneous drainage.
matory response as measured by resolute of SIRS, The optimal type of intervention depends on clini-
reduction level of circulating CRP,TNFá, or IL-6. In cal course of the patient and the precise timing of
remaining studies which compare parenteral nutrition intervention.
with jejunal feed, outcome related to infections, or- Discrimination between sterile and infected pan-
gan failure and mortality were either similar or lower. creatic necrosis:
- SAP –archetypical examples of sterile inflam-
Recommendation 9 matory process leading to organ dysfunction
Enteral nutrition should be used in preference to - the clinical picture is often one of SIRS and
parenteral nutrition in patients with SAP. can be indistinguishable from severe sepsis.
Enteral nutrition should be initiated after initial In the critical ill patients with evidence of SIRS
resuscitation. or sepsis, it is esential to discriminate between sterile
The jejunal route should be used if possible. (Grad and infected pancreatic necrosis. CT is helpful be-
A , level 1a evidence) cause the finding of retroperitoneal air is generally
indicative of the presence of gas-forming organisms
Recommendation 10 and thus, infected necrosis. In absence of retroperi-
Parenteral nutrition will be used only when at- toneal gas, ultrasound or CT-guided fine needle aspi-
tempts for enteral nutrition have failed after 5 to 7 ration (FNA) of the necrotic tissue with Gram-nega-
day trial. (Grad D, level 5 evidence) tive stain and culture can discriminate between ster-
ile and infected necrosis.
Recommendation 11 Management of infected pancreatic necrosis:
When used, parenteral nutrition should be en- - several large cases series suggest that the di-
riched with glutamine. (Grad D, level 5 evidence) agnosis of infected pancreatic necrosis warrants con-
sideration of a single or a series of intervention de-
Recommendation 12 signed to achieve the goal of a pancreatic debride-
Both enterally and parenterally fed, will be man- ment and/or drainage.
aged with protocol ensuring strict glycemic control. - there are no reports suggesting that antimicro-
(Grad A, level 1b evidence) bial therapy alone is adequate.
From more studies results that patients with SAP
Recommendation 13 and without evidence of pancreatic infection can be
No routine use of immune-enhancing enteral managed without operation with low rates of mortal-
feed formula or probiotics. (Grad D, level 5 evidence) ity and morbidity even in face of organ dysfunction.
What are the indication for surgery in SAP and The significant risk of iatrogenic bowel injuries,
what is the optimal timing for intervention? What are hemorrhage on open abdomen and infecting sterile
the roles for less invasive approach including percu- pancreatic necrosis should be considered before pro-
taneous drainage and laparoscopy? ceeding with operative debridement of sterile necro-
There are several incontrovertible indications for sis.
operative intervention in patients with SAP:
- intestinal infarct or perforation Recommendation 14
- exsanguinating hemorrhage Ultrasonographyc or CT guided FNA with Gram
- abdominal compartiment syndrome stain and culture of pancreatic or peripancreatic tis-
Routine operative of the peripancreatic fluid col- sue help to discriminate between sterile and infected

168 Timi[oara, 2005


necrosis in patients with radiological evidence of pan- Timing of billiary clearance:
creatic necrosis and clinical feature consistent with For patients with severe acute gallstones pan-
infection. (Grad C, level 4 evidence) creatitis, urgent biliary drainage and clearance of the
bile duct must be considered. There is a general con-
Recommendation 15 sensus that patients with severe acute gallstones
No debridement and/or drainage in patients with pancreatites with obstructive jaundice should undergo
sterile necrosis. (Grad C, level 4 evidence) urgent ETCP and if gallstones are identified, endo-
scopic sphincterotomy should be performed.
Recommendation 16
Debridement and/or drainage in patients with in- Recommendation 18
fected necrosis and/or abscess confirmed by radio- Gallstone pancreatitis should be suspected in all
logical evidence of gas or results of FNA. The gold patients with SAP and therefore all patients should
standard for achieving this goal is open operative de- have evaluation with sonography and biochemical
bridement. Minimally invasive techniques including tests. (Grad C, level 4 evidence)
laparoscopic and/ or percutaneous interventions might
be effective in selected patients. (Grad C, level 4 Recommendation 19
evidence) In the setting of obstructive jaundice (or other
evidence of acute obstruction of the of the biliary and/
Recommendation 17 or pancreatic tract) and acute pancreatitis due to sus-
When possible, operative necrosectomy and/or pected or confirmed gallstones, urgent ERCP should
drainage be delayed at least 2- 3 weeks to allow for be performed within 72 hours of onset of symptoms.
demarcation of the necrotic pancreas. However, the (Grad D, level 5 evidence)
clinical picture (severity and evolution) should be pri-
mary determinant of the timing of intervention. (Grad Recommendation 20
C, level 4 evidence) In the absence of obstructive jaundice, but with
Under what circumstances should patients with SAP due to suspected or confirmed gallstones, ERCP
gallstones pancreatitis undergo interventions for clear- be strongly considered within 72 hours of onset of
ance of the bile duct? symptoms. (Grad B, level 1c evidence)
Gallstones represent one of the most common Is there a role for therapy targeting the inflam-
etiologies of acute pancreatitis, accounting for 40-60%. matory response in the patients with SAP?
All patients with pancreatitis should be evaluated for The physiologic response and many of the com-
the presence of gallstones since this etiology has spe- plications of SAP occur as result of an uncontrolled
cific therapeutic implications. The mechanism by inflammatory response. Recent therapeutic strategies
which gallstones initiate the process of pancreatitis is have been directed toward interrupting the SIRS to
by temporary or persistent obstruction of the sphinc- mitigate the development of organ dysfunction. The
ter of Oddy. role of many inflammatory mediators (TNFá, IL-1â,
Given this purported mechanism, it has postu- IL-6, IL-8, PAF etc.) but there is a limited human
lated that prompt removal of stone would attenuate data. Recombinant human activated protein C
the inflammatory response. (rh-APC) has been shown to reduce mortality from
Identification for the patients with biliary pan- severe sepsis. TNFá is considered to be a key
creatitis: mediator in shock and is found in high circulating
Ultrasonography should be performed to assess concentrations in acute pancreatitis. There are no
for gallbladder stones as a potential cause of pancre- data available on its effectiveness in SAP. PAF
atitis and the abdominal CT scan should be reviewed blokade – lexipafant - PAF antagonist have been
with this in mind. shown to attenuate the inflammatory response and to
The sensitivity of ultrasound for identification of lower the incidence of organ dysfunction in two small
cholelithiasis in presence of acute pancreatitis is ap- trials. Modulation of the coagulation cascade– rh-APC
proximately 85%, whereas the sensitivity for has proven effectiveness in reducing mortality in pa-
coledocholithiasis is < 50% tients with severe sepsis.
Endoscopic ultrasound offers significantly more
sensitivity and specificity. Recommendation 21
A three-fold or greater increase in alanine ami- General supportive measure used in the critically
notransferase had a positive predictive value in iden- ill should be employed in patients with SAP as these
tifying pancreatitis with billiary etiology. interventions might play an important role in attenuat-

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ing the inflammatory response. (Grad A, level 1 b and low dose corticosteroid (Grade B level 1b evi-
evidence) dence). The careful consideration should be used
Lung – protective ventilation strategies for before administration of rh – ACP based on the theo-
patient with acute lung injury (Grad A, level1 evi- retical but unproven concern of retroperitoneal hem-
dence) orrhage. (Grad D, level 5 evidence)

Recommendation 22 Recommendation 23
Once the presence of infection is documented No use for other immuno-modulating therapies
or highly suspected and patients with SAP meet the targeting inflammatory mediators in SAP as anti-
definition of severe sepsis that management accord- TNFá therapy and lexipafant. (Grad A, level 1 evi-
ing to current sepsis guidelines be initiated. These dence for lexipafant; Grad D level 5 evidence for all
therapy include the use of rh-ACP (grade A level 1b) other therapy)

170 Timi[oara, 2005

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