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2 Diagnosis andMedical Management ofAcute Pancreatitis
25
patient is not improving clinically after 72h, CT with contrast preferably over magnetic resonance imaging (MRI) is recommended to assess for the presence of local
complications [54, 56]. If the patient meets only clinical symptoms suggestive of
pancreatitis or biochemical evidence, then a radiologic study CT imaging can also
be considered to conrm the diagnosis.
MRI and magnetic resonance cholangiopancreatography (MRCP) are used in the
diagnosis of acute pancreatitis and have higher sensitivity for diagnosis of early
pancreatitis than contrasted CT imaging [44, 54, 56]. Focal or diffuse enlargement
with blurring of the margins may be seen, failure of the pancreatic parenchyma to
enhance on a contrasted study is indicative of necrosis. MRI is considered more
useful in the effort to categorize acute uid collections and assess main pancreatic
duct anatomy and is more sensitive in diagnosis of milder forms of pancreatitis.
MRCP is better able to delineate the pancreatic and bile ducts [52, 56]. The use of
MRI may be limited due to longer scanning time, local expertise, and availability.
While not routinely used in the diagnosis of acute pancreatitis, EUS is the most
sensitive test for evaluation of small amounts of sludge or microlithiasis [57]. EUS
may be able to discern pancreatic divisum or parenchymal abnormalities and can
detect small masses that may be obscured via inammation on cross-sectional
imaging.
Patients with recurrent AP may benet from EUS for further evaluation of the
pancreatic parenchyma and ducts, or ERCP as a therapeutic modality to remove
common bile duct stones or debris [54]. Patients with unexplained pancreatitis who
are older than 40years are at an increased risk of pancreatic malignancy and should
have further imaging with CT or EUS. ERCP should be used only as a therapeutic
modality for common bile duct stone removal because it can exacerbate biliary
pancreatitis with manipulation of the pancreatic duct [39]. In cases of IAP, patients
should be referred to centers of expertise.
American College of Gastroenterology Guidelines recommend:
1. Transabdominal ultrasound should be performed in all patients with acute
pancreatitis.
2. In the absence of gallstones and/or signicant history of alcohol use, a serum
triglyceride should be obtained and considered the etiology if >1000mg/dL.
3. In a patient older than 40years, a pancreatic tumor should be considered as a
possible cause of acute pancreatitis.
4. Endoscopic investigation in patients with acute idiopathic pancreatitis should be
limited, as the risks and benets of investigation in these patients are unclear.
5. Patients with idiopathic pancreatitis should be referred to centers of expertise.
6. Genetic testing may be considered in young patients (<30years old) if no cause
is evident and a family history of pancreatic disease is present.
26
C. T. Huerta et al.
Disease Severity andClassication
There have been multiple scoring systems used over time including Apache II criteria, Bedside Index of Severity in Acute Pancreatitis (BISAP), Ranson Criteria, etc.
[58, 59]. All of these scoring systems have fallen out of favor and have been replaced
by evaluating for the presence and persistence of organ failure with presence of
SIRS criteria as a surrogate marker for this as predictors of increased morbidity and
mortality.
Risk Stratication
Use of a severity index should allow prediction of the small group of patients who
are going to develop severe disease, characterized by organ system failure, pancreatic necrosis ± infection and increased mortality. Overall mortality for AP is 2% and
increases to 30% in those with severe acute pancreatitis [43, 52]. However, others
found that the test characteristics and clinical utility if these AP severity scores
remain uncertain [60]. Investigators did not nd studies that directly assessed the
inuence of these models on patient management.
Predicting severity of AP should be simple and allow for prediction early in the
patient’s course. This is best accomplished by the BISAP or SIRS, which can predict severity within the rst 24 h. The BISAP includes blood urea nitrogen of
>25mg/dL, impaired mental status (Glasgow Coma Scale score <15), SIRS score
≥2, age >60, and pleural effusion. One point is given for each and a score of more
than three indicates an increased risk of death [58]. A follow-up evaluation by Singh
on the BISAP score reported that a score ≥3 was associated with an increased risk
of developing organ failure, persistent organ failure, and pancreatic necrosis [61].
The systemic inammatory response syndrome is dened by the presence of two
or more criteria. These consist of heart rate >90 beats/min, respiratory rate
>20breaths/min or partial pressure of carbon dioxide <32mm/hg, body temperature <36°C or >38°C, and leukocyte count <4 or >12,000 per cubic mm. Its presence during the rst 24h of admission has high sensitivity for predicting severe
disease (85%). Persistent SIRS predicted persistent organ failure in only a minority
of patients [36].
On admission, hematocrit >44% and a rise in BUN at 24h may be optional predictive tools. Reducing blood urea nitrogen and hematocrit should be used to guide
uid resuscitation over the rst 12–24h and are an accurate predictor of death [11,
62, 63]. Forsmark and Yadav noted that following serum BUN and hematocrit along
with SIRS over the rst 48h are simple and an effective scoring system to predict
severe AP (Table2.1).
2 Diagnosis andMedical Management ofAcute Pancreatitis
Table 2.1 Predictors of severe acute pancreatitis
• Patient: Age, obesity (BMI >30kg/m2), altered mental status, numerous and severe,
comorbidities including coronary artery disease, CHF, COPD, diabetes mellitus, chronic
liver disease, long history of alcohol abuse
• SIRS: Present and persists >48h
• Laboratory:
– Hematocrit >44% and no decrease with hydration,
– Urea nitrogen >20mg/dL (>7.1mmol/L), rising and/or no decrease with hydration, and/
or elevated creatinine >1.8 deciliter −159mmol/L
• Imaging: Pleural effusion or inltrates
Modied from: Bell D, etal. Medicine 43;3:174–181
Forsmark C, etal. NEJM 2016;375:1972–1981
Table 2.2 Classication of severity of acute pancreatitis
Mild Moderate Severe
Organ failure None Transient (resolves within
Local complications None Yes, without persistent
Systemic
complications
Banks PA, Bollen TL, Dervenis C, etal. GUT 2013;62:102–111
48h)
organ failure
None Yes, without persistent
organ failure
Persistent organ failure (>48h) of one
or more organs
27
Classication ofSeverity
Important revisions introduced to the Atlanta classication originally devised in
1992 have added radiographic and clinical criteria to further stratify AP into mild,
moderately severe, and severe categories [41]. Severe AP includes persistent organ
failure per the modied Marshall score criteria more than 48h compared to mild AP,
which has no associated ndings of organ failure or local or systemic complications. Moderate AP includes transient organ failure less than 48h in the presence of
local and systemic complications [41]. Moderately severe AP, as a new intermediary
category, has been further added and dened as transient organ failure less than 48h
in the presence of complications. Although it may substantially worsen underlying
comorbid diseases, moderately severe AP is associated with lower mortality compared to severe AP. Temporal phases of AP-associated complications have been
described including the propagation of end organ failure or SIRS within 1week
(early phase) and local complications manifesting after 1week (late phase). Local
complications often include pancreatic uid collections, pseudocysts, infected or
sterile wall-off necrosis, and fulminant parenchymal necrosis of the pancreas.
Necrotizing pancreatitis may include isolated peripancreatic tissue necrosis and is
often associated with infection, severe systemic end organ damage, and even mortality [64, 65] (Table2.2).
In mild AP, patients usually improve rapidly with supportive care (uid resusci-
tation) and mortality is rare, unless other severe medical comorbidities are present
28
[42, 46]. Patients with acute, mild pancreatitis by denition do not have local complications or have a modied Marshall score >2 or more that denes the presence of
organ failure (respiratory, renal, cardiovascular) [66].
Moderately severe AP is dened as the presence of transient organ system failure
(less than 48h) and/or local complications or systemic complications exacerbation
of comorbid disease without persistent organ failure [66]. Severe AP is characterized by single or multiple organ system failure >48h. These usually include respiratory, renal, and/or cardiovascular failure as measured by (systolic blood pressure
mm/hg off inotropic support) as determined by modied Marshall scoring system.
Patients with persistent SIRS >48h or infected necrosis are usually in this category
although infected necrosis can be present without organ failure.
C. T. Huerta et al.
Medical Management
Fluid Resuscitation
The cornerstone for therapy for patients with AP is judicious uid, as one of the
major sequelae of pancreatic inammation is uid sequestration. Goals of uid
therapy are to replenish lost circulatory uids to maintain organ system perfusion
and oxygenation. However, conicting evidence has been reported in the literature
with regard to the benets of aggressive uid resuscitation [46]. Sinha etal. reported
factors that independently predicted increased uid sequestration within the rst
48h after hospital admission [46] including younger age <40years, alcohol etiology, hemoconcentration, and SIRS. Increasing volumes of uid sequestration were
associated with longer hospitalizations, persistent SIRS and persistent organ system
failure [42]. Buxbaum etal. similarly reported a randomized trial of patients with
non-severe AP to aggressive (20mL/Kg Bolus followed by 3mL/Kg/h vs. standard
therapy (10mL/Kg bolus followed by 1.5mg/Kg/h) hydration with lactated Ringers
solution [67]. A signicantly higher proportion of patients treated with aggressive
uid therapy demonstrated clinical improvement compared to standard hydration.
In addition to higher volumes of uid, early uid administration correlates with
reduced morbidity among patients with AP.Gardner etal. reported that early resuscitation, dened as receipt of ≥1/3 of the total calculated 72h uid volume given
within the rst 24h of presentation, was associated with decreased development of
SIRS as well as reduced organ failure, lower rate of ICU admissions, and reduced
length of hospitalization [68, 69]. The optimal uid in this study was Ringer’s lactate [68, 69]. Clinically relevant parameters followed during uid replacement
include heart rate, urine output, and blood pressure as well as laboratory markers
such as BUN and hematocrit. Therefore, the volumes infused are based on the
patient’s hemodynamic status measured by vital signs, incorporating blood pressure, pulse and respiratory rates, age, cardiac and renal disease, laboratory values
(BUN, creatinine, and HcT) and the presence of SIRS. This “goal-directed therapy”
2 Diagnosis andMedical Management ofAcute Pancreatitis
for uid management is dened as titration of IV uids to specic clinical and biochemical targets of perfusion [68].
Fluid therapy is most effective when given early in the course of AP.This was
shown by an international, multicenter study, which found that early moderate uid
repletion (>500–1000mL) compared to non-aggressive (<500) mL uid volume
administration in the ER, was associated with lower rates of local complications
[70]. Furthermore, the aggressive uid therapy groups who received >1000mL in
the ER, also had signicantly lower need for intervention [70]. We utilize a combination of initial bolus and high-volume IV infusion (10mL/kg bolus in case of
hypovolemia, followed by 1.5mL/kg/h) and assess our goal-directed therapy using
patients’ vital signs, urine output hourly and with laboratory values (BUN, creatinine and hematocrit every 6–8h). When hemodynamic stability and laboratory values (BUN <20 and HcT <35) are reached, we decrease rates of infusion.
29
Analgesics
Abdominal pain in AP can be severe and is often the primary symptom of a are.
Moreover, failure to adequately control abdominal pain can worsen hemodynamic
instability. However, pain management in pancreatitis has been poorly studied,
leading to signicant heterogeneity both between and within different clinical practices. Adequate pain control requires a multimodal approach which may rely on the
use of intravenous opiates such as fentanyl, morphine, or hydromorphone in addition to non-opioid pain medications including acetaminophen, NSAIDs, and metamizole [44]. Epidural analgesia may also be an effective opiate sparing modality.
Among opiates, fentanyl is favorable due to its safety prole particularly in patients
with renal impairment. Although it has not been shown to incite or aggravate AP,
morphine has been known to increase sphincter of Oddi pressure and is often
avoided for this reason [44]. Historically, meperidine has been used with good efcacy; yet, it must be used cautiously due to the risk of neuromuscular irritation and
seizures caused by accumulation of the metabolite normeperidine.
Prophylactic Antibiotics
Historically, the administration of prophylactic antibiotics in patients with AP in the
past was to prevent infection and the development of necrotizing AP.Prophylactic
antibiotics were similarly thought to help address the risk of extra-pancreatic infections such as bacteremia, pneumonia, and urinary tract infections that may be
observed in up to 20% of patients with pancreatitis [65, 71]. The mortality in patients
with necrosis is up to 20% vs. interstitial AP, whose associated mortality is 5% [45,
64]. Once infection complicates necrosis, mortality increases to 30–40% [64].
Therefore, prophylactic antibiotics would appear to be a reasonable therapeutic
30
C. T. Huerta et al.
approach. However, it has been shown not to be effective in a recent Cochrane
Database systematic review of antibiotic therapy for prophylaxis against infection
of pancreatic necrosis in AP by Villatoro etal. They found that there was no benet
of antibiotics in preventing infection of pancreatic necrosis or decreasing mortality [71].
A subgroup analysis of patients in this study who received imipenem demonstrated a signicant decrease in pancreatic infections in the absence of any reduction
in mortality. Antibiotics should only be administered early in the course of patients
with AP who have suspected biliary sepsis or have extra-pancreatic infection (urinary tract infection and/or positive blood cultures) [39, 71]. Additionally, antibiotic
therapy should be reserved for suspected or diagnosed pancreatic or peripancreatic
infections in the later phase (at least 1–2weeks) after onset of disease [65]. The role
of antibiotics in this phase is to allow the focal organization of parenchymal necrosis as well as to delay surgery, usually until 4 weeks, as this is associated with
decreased mortality compared to earlier intervention [65]. Furthermore, the delay
utilization of antibiotics may allow for application of less invasive drainage procedures. As Adler and Runzi reported, antibiotic therapy alone can also effectively
treat a subgroup of patients with infected pancreatic necrosis [72, 73]. An initial
report by Runzi etal. examining nonsurgical treatment of 16 patients with severe
AP with infected pancreatic necrosis (IPN), utilized only with an antibiotic regimen
tailored to bacteriology culture results and nonsurgical therapy, reported a 12%
(2/16 patients) mortality rate [73]. Six recovered without further complications, and
10 patients developed single or multiple organ failure. This study challenged the
dogma that all patients with IPN require immediate open pancreatic surgical drainage [73]. The currently accepted management of patients with IPN is that early in
their course they can generally be managed nonsurgically with antibiotics in the
initial stage and that antibiotics alone can also be denitive therapy. The second
concept is that surgery can be delayed, which allows operative intervention to be
performed electively for more chronic sequelae of AP and with less invasive
interventions.
Nutrition
One of the goals in treating patients with AP is early enteral feeding. This should
commence as soon as the patient is hungry and ideally once nausea, emesis, and
abdominal pain are improving. Oral feeds help maintain small bowel integrity,
thereby decreasing bacterial translocation. Early gastric feeds administered via
nasogastric tube have not been shown to have signicant benets in reducing infection or death compared to oral feeding at 72h [74]. In one randomized study, over
two-thirds of patients tolerated an oral diet after its initiation at 72h after presentation, which demonstrated that starting an oral diet at 72h is not harmful to the
patient [74]. In patients with moderate or severe AP, early oral feeding once patients
demonstrate an appetite has been shown to be safe and may even shorten
2 Diagnosis andMedical Management ofAcute Pancreatitis
31
hospitalization compared to conventional oral feeding initiated after clinical and
laboratory parameters resolve [75]. Vaughn etal. in a systematic review of early
(<48h) vs. delayed (>48h) feeding in patients with AP, found that adverse events
did not increase in patients with early feeds [76]. In patients with mild to moderate
AP, early enteral feeds have been associated with a reduction in the length of hospital stay [76]. Their early nutrition group included oral as well as tube feeding.
Oral feeding intolerance (OFI), dened as relapse of symptoms following oral
feeding, occurs in approximately one of six patients with AP [77]. Predictive factors
for OFI include complicated or severe disease reected by the presence of pleural
effusion and/or peripancreatic collections. If patients have OFI, enteral nutrition
(EN) can be initiated with either nasogastric or nasojejunal feedings, as they have
similar safety proles and efcacy in these patients [77]. This should be initiated
early (<48h) in the course of severe AP and occasionally delayed for up to 72h in
patients with mild-to-moderate AP to determine if they can tolerate oral feeding.
Low rates of infusion possibly decrease bowel permeability, but the goal should aim
to meet patients’ caloric demands. Enteral nutrition should be started prior to 48h
in patients with severe pancreatitis, especially those who are intubated. Khaled etal.
showed that benets of early feeding were more evident in the sickest (treated with
multiple vasopressors) ICU patients [77].
Bakker OJ reported a meta-analysis of 165 individuals from 8 randomized trials
[78]. The cohort was divided into those who received EN within 24h of admission
vs. those who received EN after 24h of admission. Those receiving EN within 24h
of admission had decreased organ failure, 42 vs. 16% (OR 0.42), and a reduction in
the complications of infected pancreatic necrosis and/or organ failure. No difference in mortality was observed and earlier initiation of EN was deemed better for
patients with severe AP.However, benets of EN begun within 3days could reduce
the risk of secondary infection and improve the nutritional status of patients with
AP [78].
Overall, enteral nutrition should be utilized over parenteral nutrition in patients
with AP.Enteral nutrition has a multitude of advantages over parenteral nutrition
including avoidance of complications of invasive central venous access procedures,
catheter-related sepsis, lower cost, maintenance of enteral barrier function, and
decreasing bacterial translocation, which is a critical factor in the evolution of infections in AP patients [79, 80]. Enteral vs. parenteral nutrition results in reduction in
the risk of total and pancreatic infectious complications and risk of death [79, 80].
Complications
Most patients with AP experience acute interstitial edematous pancreatitis, which is
mild in severity with resolution in 3–5days without complications [45]. Twenty
percent experience moderately severe or severe acute pancreatitis with local or systemic complications [45]. Local complications of AP include peripancreatic collections such as acute uid collections, pseudocysts, acute necrotic collections, and
32
C. T. Huerta et al.
walled-off necrosis [81]. Acute peripancreatic uid collections and acute necrotic
collections usually develop within 4weeks of an episode of AP, while pseudocysts
and walled-off necrosis usually occur after 4weeks once there is maturation of a
wall [81]. Necrotic collections have tissue debris as well as uid contents, whereas
acute uid collections and pseudocysts only have uid contents. Approximately
50% of patients with necrotizing AP will develop portosplenomesenteric thrombosis, which is uncommon in the absence of necrosis [82]. Contrast-enhanced CT scan
to investigate for the presence of necrosis should be considered in patients who fail
to respond to supportive management after 72h [52]. Pancreatic necrosis should be
managed conservatively with a step-up approach focusing on supportive care measures, followed by catheter drainage if there are ongoing symptoms or a need for
drainage of infected necrosis. Interventions with EUS or a minimally invasive surgical approach should be considered for those patients with walled-off infected necrosis who are not clinically improving despite antibiotic treatment [55]. The advent of
procedures such as EUS-guided placement of lumen apposing metal stents (LAMS)
has enabled cyst-gastrostomy of uid collections with immediate drainage, and
endoscopic necrosectomy for walled-off necrosis [53]. Timing of the intervention is
of utmost importance, and treatment should be delayed for at least 3–4weeks after
the initial episode of AP to allow for maturation of uid collection walls and to
enable delineation of tissue planes. Open necrosectomy should be reserved for
severe refractory cases in which minimally invasive approaches fail, as this operation is associated with signicant complications and an overall poor prognosis
[45, 47].
Systemic complications of AP are dened according to the revised Atlanta classication as an exacerbation of an underlying comorbidity [41]. Such conditions
may include coronary artery disease or chronic lung disease. Organ failure is a distinct entity related to activation of a cytokine cascade from acute pancreatic inammation, which results in SIRS [36]. SIRS may lead to organ failure of one or more
organ systems leading to renal failure, shock, and respiratory failure and is the
major cause of death due to acute pancreatitis [36]. Patients may also develop complications of hypocalcemia and other metabolic abnormalities, blindness, pseudocysts, necrosis, hemorrhage, and multisystem organ failure. Long-term, if there is
disruption with disconnection of the pancreatic duct due to an episode of acute
pancreatitis, this may lead to recurrent complications including uid collections as
well as exocrine pancreatic insufciency [43].
Long-Term Sequelae of Acute Pancreatitis
Patients who have recovered from AP are at signicant risk for recurrence if the
initial cause has not been elucidated and corrected. The morbidity of a bout of AP
persists in some patients after recovery of AP.An episode of AP increases a patient’s
risk of developing diabetes mellitus, progressing to chronic pancreatitis with exocrine pancreatic insufciency and is associated with an increased risk of harboring
2 Diagnosis andMedical Management ofAcute Pancreatitis
33
or developing pancreatic cancer [32, 81]. Patients who had severe AP that required
critical care were found to have a high risk for developing new onset of diabetes
mellitus. Therefore, multidisciplinary management of these patients and ensuring
follow-up with gastroenterology is crucial.
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